MetaFilter posts tagged with microbiology

The rise of the tick

Blasdelb — Thu, 02 May 2013 09:28:57 -0800

With incisor-like claws that can tunnel beneath your skin in seconds, ticks are rapidly establishing themselves as the Swiss Army knife of disease vectors. Carl Zimmer walks into the woods to find out why these tiny beasts appear to be skyrocketing in number – and outsmarting environmental scientists trying to control them with every bite.

Silicon-based viruses of the analog kind

Blazecock Pileon — Tue, 09 Apr 2013 16:08:21 -0800

A selection of glass viruses by artist Luke Jerram (a full gallery and photographs of other sculptural work are also available directly from his site)

Parasite of the Day

Blasdelb — Mon, 18 Feb 2013 07:04:26 -0800

Does just what it says on the tin,

"So, naturalists observe, a flea has smaller fleas that on him prey; and these have smaller still to bite ’em; and so proceed ad infinitum." - Jonathan Swift

The Unsettling Beauty of Lethal Viruses

heyho — Fri, 08 Feb 2013 13:58:05 -0800

“Viruses have no color as they are smaller than the wavelength of light,” says Jerram, in an email. “So the artworks are created as alternative representations of viruses to the artificially colored imagery we receive through the media.” Jerram and Davidson create sketches, which they then take to the glassblowers, to see whether the intricate structures of the diseases can be replicated in glass, at approximately one million times their original size. RECENTLY

The answer, my friend, is blowing in the wind: E. Coli & Cloud Formation

y2karl — Tue, 29 Jan 2013 01:13:03 -0800

Scientists Find Bacteria Survive at High Altitudes
Study finds significant microorganism populations in middle and upper troposphere
Microbiome of the upper troposphere: Species composition and prevalence, effects of tropical storms, and atmospheric implications
See also Properties of biological aerosols and their impact on atmospheric processes

Slow Motion Sneezing

Blasdelb — Sat, 26 Jan 2013 08:22:15 -0800

Sneezing in Slow Motion; somehow simultaneously more fascinating, terrifying, and disgusting than you'd imagine it'd be. Curtesy of the South Australian Health's youtube channel Some fun light reading:

“Gesundheit!” Sneezing, Common Colds, Allergies, and Staphylococcus aureus Dispersion Background: Staphylococcus aureus is among the most important pathogens in today’s hospital setting Methods: The effects of sneezing on the airborne dispersal of S. aureus and other bacteria were assessed in 11 healthy nasal S. aureus carriers with experimentally induced rhinovirus colds. Airborne dispersal was studied by volumetric air sampling in 2 chamber sessions with and without histamine-induced sneezing. After 2 days of preexposure measurements, volunteers were inoculated with a rhinovirus and monitored for 14 days. Daily quantitative nasal- and skin-culture samples for bacteria and nasal-culture samples for rhinovirus were obtained, cold symptoms were assessed, and volunteer activities were recorded during sessions Results: All participants developed a cold. Sneezing caused a 4.7-fold increase in the airborne dispersal of S. aureus a 1.4-fold increase in coagulase-negative staphylococci (CoNS), and a 3.9-fold increase in other bacteria (P<>Conclusion: Nasal S. aureus carriers disperse a significant amount of S. aureus into the air by sneezing. Experimental colds do not alter bacterial dispersal, but respiratory allergies multiply the effect of dispersing S. aureus

The A-Z of Epidemiology:

Blasdelb — Mon, 21 Jan 2013 15:18:16 -0800

Germs from Anthrax to Zoonoses. A disturbing bedtime book for kids. In order:

Anthrax (previously) Botulism (previously) Chlamydia (previously) Diphtheria Ebola Food Poisoning Giardia Herpes Intestines John Snow MD Klebsiella Legionella Measels Norovirus (previously) Opportunistic Pathogen Petri Dish Q Fever Rabies Swine Flu Trichinosis (previously) Urine (an exhaustive report of what is in urine and what it can do to you, NASA Contractor Report No. NASA CR-1802, D. F. Putnam, July 1971 (PDF)) Veins Washing Xylella Yersinia Zoonoses

Viruses That Make Zombies and Vaccines

Blasdelb — Sat, 19 Jan 2013 01:46:34 -0800

This week the FDA announced that they were approving a new kind of flu vaccine. Nestled in the articles was an odd fact: unlike traditional flu vaccines, the new kind, called Flublok, is produced by the cells of insects. This is the kind of detail that you might skim over without giving it a thought. If you did pause to ponder, you might be puzzled: how could insects possibly make a vaccine against viruses that infect humans? The answer may surprise you. To make vaccines, scientists are tapping into a battle between viruses and insects that’s raging in forests and fields and backyards all around us. It’s an important lesson in how to find new ideas in biotechnology: first, leave biologists free to explore the weirdest corners of nature they can find. How a zombie virus became a big biotech business Also by Zimmer Liquefying virus uses one gene to make caterpillars climb By Ed Yong of Not Exactly Rocket Science

Toward system-level understanding of baculovirus–host cell interactions: from molecular fundamental studies to large-scale proteomics approaches Baculoviruses are insect viruses extensively exploited as eukaryotic protein expression vectors. Molecular biology studies have provided exciting discoveries on virus–host interactions, but the application of omic high-throughput techniques on the baculovirus–insect cell system has been hampered by the lack of host genome sequencing. While a broader, systems-level analysis of biological responses to infection is urgently needed, recent advances on proteomic studies have yielded new insights on the impact of infection on the host cell. These works are reviewed and critically assessed in the light of current biological knowledge of the molecular biology of baculoviruses and insect cells.

So high, so low, so many things to know.

zarq — Tue, 08 Jan 2013 14:20:09 -0800

Woese once said of himself and his work that when a wise man points out the moon, only a fool looks at the finger. Let us all be fools if just for a moment .

Blasdelb — Wed, 02 Jan 2013 07:29:30 -0800

Microbiology's Scarred Revolutionary^(PDF), Carl Woese (pron.: /ˈwoʊz/), a biophysicist and evolutionary microbiologist whose discovery 35 years ago of a “third domain” of life in the vast realm of micro-organisms altered scientific understanding of evolution, died on Sunday at his home in Urbana, Ill. He was 84. “Imagine walking out in the countryside and not being able to tell a snake from a cow from a mouse from a blade of grass, that’s been the level of our ignorance.”-Woese

Carl Woese's distinguished career was dominated by his idea that divisions between different kinds of living organisms could be better defined by their small subunit ribosomal RNA^{(smaller bottom piece here)} sequences than by their morphology, biochemistry, outer membrane, or even necessarily the most basic of divisions like multicellularity or the presence of cellular organelles. Indeed, seeing life through this much clearer lens, he was able to show that the microbes known as Archaea are at least as different from Bacteria as they are from Eukaryotes like plants and animals, a finding he presented here to much controversy and derision:
Woese, Carl R.; George E. Fox (1977). "Phylogenetic structure of the prokaryotic domain: the primary kingdoms.^(PDF)". Proceedings of the National Academy of Sciences of the United States of America 74 (11): 5088–5090 A phylogenetic analysis based upon ribosomal RNA sequence characterization reveals that living systems represent one of three aboriginal lines of descent: (i) the eubacteria, comprising all typical bacteria; (ii) the archaebacteria, containing methanogenic bacteria; and (iii) the eurkaryotes, now represented in the cytoplasmic component of eukaryotic cells.
Fought for eloquently here:
Woese, Carl R. (1987-06-01). "Bacterial evolution.^(PDF)". Microbiological Reviews 51 (2): 221–271 A revolution is occurring in biology: perhaps it is better characterized as a revolution within a revolution. I am, of course, referring to the impact that the increasingly rapid capacity to sequence nucleic acids is having on a science that has already been radically transformed by molecular approaches and concepts. While the impact is currently greatest in genetics and applied areas such as medicine and biotechnology, its most profound and lasting effect will be on our perception of evolution and its relationship to the rest of biology. The cell is basically an historical document, and gaining the capacity to read it (by the sequencing of genes) cannot but drastically alter the way we look at all of biology. No discipline within biology will be more changed by this revolution than microbiology, for until the advent of molecular sequencing, bacterial evolution was not a subject that could be approached experimentally. With any novel scientific departure it is important to understand the historical setting in which it arises-the paradigm it will change. Old prejudices tend to inhibit, distort, or otherwise shape new ideas, and historical analysis helps to eliminate much of the negative impact of the status quo. Stch analysis is particularly importaht in the present instance since microbiologists do not deal with evolutionary considerations as a matter of course and so tend not to appreciate them. Therefore, I begin this discussion with a brief look at how the relationship between microbiology and evolution (i.e., the lack thereof) developed.
And presented again thirteen years later, this time as core scientific dogma:
Woese, C R; O Kandler, M L Wheelis (1990). "Towards a natural system of organisms: proposal for the domains Archaea, Bacteria, and Eucarya.^(PDF)". Proceedings of the National Academy of Sciences of the United States of America 87 (12): 4576–4579. Molecular structures and sequences are generally more revealing of evolutionary relationships than are classical phenotypes (particularly so among microorganisms). Consequently, the basis for the definition of taxa has progressively shifted from the organismal to the cellular to the molecular level. Molecular comparisons show that life on this planet divides into three primary groupings, commonly known as the eubacteria, the archaebacteria, and the eukaryotes. The three are very dissimilar, the differences that separate them being of a more profound nature than the differences that separate typical kingdoms, such as animals and plants. Unfortunately, neither of the conventionally accepted views of the natural relationships among living systems--i.e., the five-kingdom taxonomy or the eukaryote-prokaryote dichotomy--reflects this primary tripartite division of the living world. To remedy this situation we propose that a formal system of organisms be established in which above the level of kingdom there exists a new taxon called a "domain." Life on this planet would then be seen as comprising three domains, the Bacteria, the Archaea, and the Eucarya, each containing two or more kingdoms. (The Eucarya, for example, contain Animalia, Plantae, Fungi, and a number of others yet to be defined). Although taxonomic structure within the Bacteria and Eucarya is not treated herein, Archaea is formally subdivided into the two kingdoms Euryarchaeota (encompassing the methanogens and their phenotypically diverse relatives) and Crenarchaeota (comprising the relatively tight clustering of extremely thermophilic archaebacteria, whose general phenotype appears to resemble most the ancestral phenotype of the Archaea.

“It’s clear to me that if you wiped all multicellular life-forms off the face of the earth, microbial life might shift a tiny bit, if microbial life were to disappear, that would be it — instant death for the planet.”-Woese

Later in life he became something of an elder statesman of evolutionary microbiology publishing the occasional review:
Woese, Carl R.; Nigel Goldenfeld (2009). "How the Microbial World Saved Evolution from the Scylla of Molecular Biology and the Charybdis of the Modern Synthesis". Microbiology and Molecular Biology Reviews 73 (1): 14–21. In this commentary, we provide a personal overview of the conceptual history of microbiology and molecular biology over the course of the last hundred years, emphasizing the relationship of these fields to the problem of evolution. We argue that despite their apparent success, all three reached an impasse that arose from the influence of dogmatic or overly narrow perspectives. Finally, we describe how recent developments in microbiology are realizing Beijerinck's vision of a field that is fully integrated with molecular biology, microbial ecology, thereby challenging and extending current thinking in evolution.

Today, whenever a student of biology opens their textbook what they see first is a blown up image of the tripartite tree of life – a small tribute to a man and a discovery that changed our view of nature forever."

Deciphering the Tools of Nature’s Zombies

Blasdelb — Sun, 09 Dec 2012 07:21:57 -0800

Deciphering the Tools of Nature’s Zombies: The ability of parasites to alter the behaviour of their hosts fascinates both scientists and non-scientists alike. One reason that this topic resonates with so many is that it touches on core philosophical issues such as the existence of free will. If the mind is merely a machine, then it can be controlled by any entity that understands the code and has access to the machinery. This special issue of The Journal of Experimental Biology highlights some of the best-understood examples of parasite-induced changes in host brain and behaviour, encompassing both invertebrate and vertebrate hosts and micro- and macro-parasites. Full issue annotated inside: AN INTRODUCTION:

HOW PERNICIOUS PARASITES TURN VICTIMS INTO ZOMBIES Parasites come in all shapes and forms. From skinny tapeworms that infest intestines to the microscopic infectious agent of malaria (Plasmodium), parasites are usually inconvenient and sometimes lethal. But there is one group of parasites that is particularly pernicious – they are the parasites that hijack their host’s nervous system, turning their victims into zombies. ‘The fact that parasites can so efficiently alter host behaviour is fascinating’, says JEB Editor Michael Dickinson, from the University of Washington, USA, adding, ‘There is something horrifying and wondrous about a tiny “implant” being able to control such a large animal machine’. What is more, it appears that these minute manipulators can have a significant, and often under-appreciated, impact on ecology, physiology and evolution, orchestrating the behaviour of vertebrates and invertebrates alike. ‘Neuroparasitology is a science where science meets science fiction’, Dickinson observes. However, the community tackling the thorny question of how parasites take possession of their hosts by manipulating their nervous systems, and the large-scale implications of these behavioural changes, is tiny. Shelley Adamo – an insect behavioural physiologist from Dalhousie University, Canada – adds that working with parasitic systems is particularly challenging because of the necessity of raising two different organisms in the lab. ...

ALTERATION OF HOST BEHAVIOR

Parasites: evolution’s neurobiologists For millions of years, parasites have altered the behaviour of their hosts. Parasites can affect host behaviour by: (1) interfering with the host’s normal immune–neural communication, (2) secreting substances that directly alter neuronal activity via non-genomic mechanisms and (3) inducing genomic- and/or proteomic-based changes in the brain of the host. Changes in host behaviour are often restricted to particular behaviours, with many other behaviours remaining unaffected. Neuroscientists can produce this degree of selectivity by targeting specific brain areas. Parasites, however, do not selectively attack discrete brain areas. Parasites typically induce a variety of effects in several parts of the brain. Parasitic manipulation of host behaviour evolved within the context of the manipulation of other host physiological systems (especially the immune system) that was required for a parasite’s survival. This starting point, coupled with the fortuitous nature of evolutionary innovation and evolutionary pressures to minimize the costs of parasitic manipulation, likely contributed to the complex and indirect nature of the mechanisms involved in host behavioural control. Because parasites and neuroscientists use different tactics to control behaviour, studying the methods used by parasites can provide novel insights into how nervous systems generate and regulate behaviour. Studying how parasites influence host behaviour will also help us integrate genomic, proteomic and neurophysiological perspectives on behaviour. An overview of parasite-induced behavioral alterations – and some lessons from bats An animal with a parasite is not likely to behave like a similar animal without that parasite. This is a simple enough concept, one that is now widely recognized as true, but if we move beyond that statement, the light that it casts on behavior fades quickly: the world of parasites, hosts and behavior is shadowy, and boundaries are ill-defined. For instance, at first glance, the growing list of altered behaviors tells us very little about how those alterations happen, much less how they evolved. Some cases of parasite-induced behavioral change are truly manipulative, with the parasite standing to benefit from the changed behavior. In other cases, the altered behavior has an almost curative, if not prophylactic, effect; in those cases, the host benefits. This paper will provide an overview of the conflicting (and coinciding) demands on parasite and host, using examples from a wide range of taxa and posing questions for the future. In particular, what does the larger world of animal behavior tell us about how to go about seeking insights – or at least, what not to do? By asking questions about the sensory–perceptual world of hosts, we can identify those associations that hold the greatest promise for neuroethological studies of parasite-induced behavioral alterations, and those studies can, in turn, help guide our understanding of how parasite-induced alterations evolved, and how they are maintained. Parasite manipulation of host personality and behavioural syndromes The past decades have seen mounting evidence that parasites alter their host’s behaviour in ways that benefit transmission, based on differences in the expression of behavioural traits between infected and control individuals, or on significant correlations between trait expression and infection levels. The multidimensional nature of host manipulation has only recently been recognised: parasites do not target single host traits, but instead suites of interrelated traits. Here, I use recent research on animal personality (behavioural differences among individuals consistent across time and situations) and behavioural syndromes (correlations at the population level among distinct behavioural traits, or between the same trait expressed in different contexts) to provide a framework from which simple testable patterns of host behavioural changes can be predicted. Following infection, a manipulative parasite could (i) change the temporal consistency of its host’s behavioural responses, (ii) change the slope of a host reaction norm, i.e. the way host behavioural traits are expressed as a function of an environmental gradient, or (iii) decouple two or more host behavioural traits and/or change the way in which they correlate with each other. Two case studies involving trematode parasites and their freshwater hosts are used to provide empirical illustrations of the above scenarios. These clearly illustrate the full richness of behavioural alterations induced by parasites, and how these effects would go unnoticed using the classical trait-by-trait comparisons of mean values between parasitised and non-parasitised individuals. However, the power of animal personality and behavioural syndromes to inform research on host manipulation by parasites will only be fully realised when underlying mechanisms are elucidated and linked to their phenotypic impacts. Multidimensionality in parasite-induced phenotypic alterations: ultimate versus proximate aspects In most cases, parasites alter more than one dimension in their host phenotype. Although multidimensionality in parasite-induced phenotypic alterations (PIPAs) ^{[FULL TEXT]} seems to be the rule, it has started to be addressed only recently. Here, we critically review some of the problems associated with the definition, quantification and interpretation of multidimensionality in PIPAs. In particular, we confront ultimate and proximate accounts, and evaluate their own limitations. We end up by introducing several suggestions for the development of future research, including some practical guidelines for the quantitative analysis of multidimensionality in PIPAs. Diversity and evolution of bodyguard manipulation Among the different strategies used by parasites to usurp the behaviour of their host, one of the most fascinating is bodyguard manipulation. While all classic examples of bodyguard manipulation involve insect parasitoids, induced protective behaviours have also evolved in other parasite–host systems, typically as specific dimensions of the total manipulation. For instance, parasites may manipulate the host to reduce host mortality during their development or to avoid predation by non-host predators. This type of host manipulation behaviour is rarely described, probably due to the fact that studies have mainly focused on predation enhancement rather than studying all the dimensions of the manipulation. Here, in addition to the classic cases of bodyguard manipulation, we also review these ‘bodyguard dimensions’ and propose extending the current definition of bodyguard manipulation to include the latter. We also discuss different evolutionary scenarios under which such manipulations could have evolved. How much energy should manipulative parasites leave to their hosts to ensure altered behaviours? Although host manipulation is likely to be costly for parasites, we still have a poor understanding of the energetic aspects underlying this strategy. It is traditionally assumed that physiological costs are inevitably associated with mechanisms evolved by parasites to induce the required changes in host behaviours. While most energetic expenditures of parasites relate primarily to bringing about the altered behaviours, manipulative parasites also have to consider the condition of their host during the manipulation. Here, we suggest that because of this trade-off, the energy required to accomplish parasite-induced behaviours may represent a key energetic constraint for parasites. Depending on the energetic expenditures specific to each type of manipulation, parasites should undergo selection to secure resources for their host to allow them to perform manipulated behaviours. What can parasitoid wasps teach us about decision-making in insects? Millions of years of co-evolution have driven parasites to display very complex and exquisite strategies to manipulate the behaviour of their hosts. However, although parasite-induced behavioural manipulation is a widespread phenomenon, the underlying neuronal mechanisms are only now beginning to be deciphered. Here, we review recent advancements in the study of the mechanisms by which parasitoid wasps use chemical warfare to manipulate the behaviour of their insect hosts. We focus on a particular case study in which a parasitoid wasp (the jewel wasp Ampulex compressa) performs a delicate brain surgery on its prey (the American cockroach Periplaneta americana) to take away its motivation to initiate locomotion. Following a brief background account of parasitoid wasps that manipulate host behaviour, we survey specific aspects of the unique effects of the A. compressa venom on the regulation of spontaneous and evoked behaviour in the cockroach host.
(Big awesome post about parasitoid wasps previously: The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes.)
Comparing mechanisms of host manipulation across host and parasite taxa Parasites affect host behavior in several ways. They can alter activity, microhabitats or both. For trophically transmitted parasites (the focus of our study), decreased activity might impair the ability of hosts to respond to final-host predators, and increased activity and altered microhabitat choice might increase contact rates between hosts and final-host predators. In an analysis of trophically transmitted parasites, more parasite groups altered activity than altered microhabitat choice. Parasites that infected vertebrates were more likely to impair the host’s reaction to predators, whereas parasites that infected invertebrates were more likely to increase the host’s contact with predators. The site of infection might affect how parasites manipulate their hosts. For instance, parasites in the central nervous system seem particularly suited to manipulating host behavior. Manipulative parasites commonly occupy the body cavity, muscles and central nervous systems of their hosts. Acanthocephalans in the data set differed from other taxa in that they occurred exclusively in the body cavity of invertebrates. In addition, they were more likely to alter microhabitat choice than activity. Parasites in the body cavity (across parasite types) were more likely to be associated with increased host contact with predators. Parasites can manipulate the host through energetic drain, but most parasites use more sophisticated means. For instance, parasites target four physiological systems that shape behavior in both invertebrates and vertebrates: neural, endocrine, neuromodulatory and immunomodulatory. The interconnections between these systems make it difficult to isolate specific mechanisms of host behavioral manipulation.

NEUROIMMUNOLOGY

Parasite-induced alterations of sensorimotor pathways in gammarids: collateral damage of neuroinflammation? Some larval helminths alter the behavior of their intermediate hosts in ways that favor the predation of infected hosts, thus enhancing trophic transmission. Gammarids (Crustacea: Amphipoda) offer unique advantages for the study of the proximate factors mediating parasite-induced behavioral changes. Indeed, amphipods infected by distantly related worms (acanthocephalans, cestodes and trematodes) encysted in different microhabitats within their hosts (hemocoel, brain) present comparable, chronic, behavioral pathologies. In order to evaluate the potential connection between behavioral disturbances and immune responses in parasitized gammarids, this Review surveys the literature bearing on sensorimotor pathway dysfunctions in infected hosts, on the involvement of the neuromodulator serotonin in altered responses to environmental stimuli, and on systemic and neural innate immunity in arthropods. Hemocyte concentration and phenoloxidase activity associated with melanotic encapsulation are depressed in acanthocephalan-manipulated gammarids. However, other components of the arsenal deployed by crustaceans against pathogens have not yet been investigated in helminth-infected gammarids. Members of the Toll family of receptors, cytokines such as tumor necrosis factors (TNFs), and the free radical nitric oxide are all implicated in neuroimmune responses in crustaceans. Across animal phyla, these molecules and their neuroinflammatory signaling pathways are touted for their dual beneficial and deleterious properties. Thus, it is argued that neuroinflammation might mediate the biochemical events upstream of the serotonergic dysfunction observed in manipulated gammarids – a parsimonious hypothesis that could explain the common behavioral pathology induced by distantly related parasites, both hemocoelian and cerebral. The significance of cerebral toxocariasis: a model system for exploring the link between brain involvement, behaviour and the immune response Toxocara canis is a parasitic nematode that infects canines worldwide, and as a consequence of the widespread environmental dissemination of its ova in host faeces, other abnormal hosts including mice and humans are exposed to infection. In such abnormal or paratenic hosts, the immature third-stage larvae undergo a somatic migration through the organs of the body but fail to reach maturity as adult worms in the intestine. The presence of the migrating larvae contributes to pathology that is dependent upon the intensity of infection and the location of the larvae. A phenomenon of potential public health significance in humans and of ecological significance in mice is that T. canis larvae exhibit neurotrophic behaviour, which results in a greater concentration of parasites in the brain, as infection progresses. Toxocara larval burdens vary between individual outbred mice receiving the same inocula, suggesting a role for immunity in the establishment of cerebral infection. Although the systemic immune response to T. canis has been widely reported, the immune response in the brain has received little attention. Differential cytokine expression and other brain injury-associated biomarkers have been observed in infected versus uninfected outbred and inbred mice. Preliminary data have also suggested a possible link between significant memory impairment and cytokine production associated with T. canis infection. Mice provide a useful, replicable animal model with significant applicability and ease of manipulation. Understanding the cerebral host–parasite relationship may shed some light on the cryptic symptoms of human infection where patients often present with other CNS disorders such as epilepsy and mental retardation. Immune–neural connections: how the immune system’s response to infectious agents influences behavior Humans and animals use the classical five senses of sight, sound, touch, smell and taste to monitor their environment. The very survival of feral animals depends on these sensory perception systems, which is a central theme in scholarly research on comparative aspects of anatomy and physiology. But how do all of us sense and respond to an infection? We cannot see, hear, feel, smell or taste bacterial and viral pathogens, but humans and animals alike are fully aware of symptoms of sickness that are caused by these microbes. Pain, fatigue, altered sleep pattern, anorexia and fever are common symptoms in both sick animals and humans. Many of these physiological changes represent adaptive responses that are considered to promote animal survival, and this constellation of events results in sickness behavior. Infectious agents display a variety of pathogen-associated molecular patterns (PAMPs) that are recognized by pattern recognition receptors (PRRs). These PRR are expressed on both the surface [e.g. Toll-like receptor (TLR)-4] and in the cytoplasm [e.g. nucleotide-binding oligomerization domain (Nod)-like receptors] of cells of the innate immune system, primarily macrophages and dendritic cells. These cells initiate and propagate an inflammatory response by stimulating the synthesis and release of a variety of cytokines. Once an infection has occurred in the periphery, both cytokines and bacterial toxins deliver this information to the brain using both humoral and neuronal routes of communication. For example, binding of PRR can lead to activation of the afferent vagus nerve, which communicates neuronal signals via the lower brain stem (nucleus tractus solitarius) to higher brain centers such as the hypothalamus and amygdala. Blood-borne cytokines initiate a cytokine response from vascular endothelial cells that form the blood–brain barrier (BBB). Cytokines can also reach the brain directly by leakage through the BBB via circumventricular organs or by being synthesized within the brain, thus forming a mirror image of the cytokine milieu in the periphery. Although all cells within the brain are capable of initiating cytokine secretion, microglia have an early response to incoming neuronal and humoral stimuli. Inhibition of proinflammatory cytokines that are induced following bacterial infection blocks the appearance of sickness behaviors. Collectively, these data are consistent with the notion that the immune system communicates with the brain to regulate behavior in a way that is consistent with animal survival.

TOXOPLASMOSIS

Toxoplasma gondii infection, from predation to schizophrenia: can animal behaviour help us understand human behaviour? We examine the role of the protozoan Toxoplasma gondii as a manipulatory parasite and question what role study of infections in its natural intermediate rodent hosts and other secondary hosts, including humans, may elucidate in terms of the epidemiology, evolution and clinical applications of infection. In particular, we focus on the potential association between T. gondii and schizophrenia. We introduce the novel term ‘T. gondii–rat manipulation–schizophrenia model’ and propose how future behavioural research on this model should be performed from a biological, clinical and ethically appropriate perspective. Toxoplasma gondii infection and behaviour – location, location, location? Parasite location has been proposed as an important factor in the behavioural changes observed in rodents infected with the protozoan Toxoplasma gondii. During the chronic stages of infection, encysted parasites are found in the brain but it remains unclear whether the parasite has tropism for specific brain regions. Parasite tissue cysts are found in all brain areas with some, but not all, prior studies reporting higher numbers located in the amygdala and frontal cortex. A stochastic process of parasite location does not, however, seem to explain the distinct and often subtle changes observed in rodent behaviour. One factor that could contribute to the specific changes is increased dopamine production by T. gondii. Recently, it was found that cells encysted with parasites in the brains of experimentally infected rodents have high levels of dopamine and that the parasite encodes a tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of this neurotransmitter. A mechanism is proposed that could explain the behaviour changes due to parasite regulation of dopamine. This could have important implications for T. gondii infections in humans. Parasite-augmented mate choice and reduction in innate fear in rats infected by Toxoplasma gondii Typically, female rats demonstrate clear mate choice. Mate preference is driven by the evolutionary need to choose males with heritable parasite resistance and to prevent the transmission of contagious diseases during mating. Thus, females detect and avoid parasitized males. Over evolutionary time scales, parasite-free males plausibly evolve to advertise their status. This arrangement between males and females is obviously detrimental to parasites, especially for sexually transmitted parasites. Yet Toxoplasma gondii, a sexually transmitted parasite, gets around this obstacle by manipulating mate choice of uninfected females. Males infected with this parasite become more attractive to uninfected females. The ability of T. gondii to not only advantageously alter the behavior and physiology of its host but also secondarily alter the behavior of uninfected females presents a striking example of the ‘extended phenotype’ of parasites. Toxoplasma gondii also abolishes the innate fear response of rats to cat odor; this likely increases parasite transmission through the trophic route. It is plausible that these two manipulations are not two distinct phenotypes, but are rather part of a single pattern built around testosterone-mediated interplay between mate choice, parasitism and predation. Influence of latent Toxoplasma infection on human personality, physiology and morphology: pros and cons of the Toxoplasma–human model in studying the manipulation hypothesis The parasitic protozoan Toxoplasma gondii infects about one-third of the population of developed countries. The life-long presence of dormant stages of this parasite in the brain and muscular tissues of infected humans is usually considered asymptomatic from the clinical point of view. In the past 20 years, research performed mostly on military personnel, university students, pregnant women and blood donors has shown that this ‘asymptomatic’ disease has a large influence on various aspects of human life. Toxoplasma-infected subjects differ from uninfected controls in the personality profile estimated with two versions of Cattell’s 16PF, Cloninger’s TCI and Big Five questionnaires. Most of these differences increase with the length of time since the onset of infection, suggesting that Toxoplasma influences human personality rather than human personality influencing the probability of infection. Toxoplasmosis increases the reaction time of infected subjects, which can explain the increased probability of traffic accidents in infected subjects reported in three retrospective and one very large prospective case-control study. Latent toxoplasmosis is associated with immunosuppression, which might explain the increased probability of giving birth to a boy in Toxoplasma-infected women and also the extremely high prevalence of toxoplasmosis in mothers of children with Down syndrome. Toxoplasma-infected male students are about 3 cm taller than Toxoplasma-free subjects and their faces are rated by women as more masculine and dominant. These differences may be caused by an increased concentration of testosterone. Toxoplasma also appears to be involved in the initiation of more severe forms of schizophrenia. At least 40 studies confirmed an increased prevalence of toxoplasmosis among schizophrenic patients. Toxoplasma-infected schizophrenic patients differ from Toxoplasma-free schizophrenic patients by brain anatomy and by a higher intensity of the positive symptoms of the disease. Finally, five independent studies performed in blood donors, pregnant women and military personnel showed that RhD blood group positivity, especially in RhD heterozygotes, protects infected subjects against various effects of latent toxoplasmosis, such as the prolongation of reaction times, an increased risk of traffic accidents and excessive pregnancy weight gain. The modern human is not a natural host of Toxoplasma. Therefore, it can only be speculated which of the observed effects of latent toxoplasmosis are the result of the manipulation activity of the Toxoplasma aimed to increase the probability of its transmission from a natural intermediate to the definitive host by predation, and which are just side effects of chronic infection.

NEW APPROACHES

Investigating candidate neuromodulatory systems underlying parasitic manipulation: concepts, limitations and prospects Studies addressing the functional basis of parasitic manipulation suggest that alteration of the neuromodulatory system is a common feature of manipulated hosts. Screening of the neuromodulatory system has so far been carried out by performing ethopharmacological analysis, biochemical quantification of neurotransmitters and neuromodulators, and/or immunocytochemistry. Here, we review the advantages and limitations of such approaches through the analysis of case studies. We further address whether the analysis of candidate neuromodulatory systems fits the current view of manipulation as being multidimensional. The benefits in combining ethopharmacology with more recent molecular tools to investigate candidate neuromodulatory pathways is also emphasized. We conclude by discussing the value of a multidisciplinary study of parasitic manipulation, combining evolutionary (parasite transmission), behavioural (syndrome of manipulation) and neuroimmunological approaches. Pathways to understanding the extended phenotype of parasites in their hosts The study of the adaptive manipulation of animal behavior by parasites is entering very exciting times. Collectively the field has moved from its important and instructional natural history phase into proximate-level studies aiming to elucidate the mechanisms by which one organism controls another. Because many cases studies involve cross-kingdom control of behaviour, the findings are sure to be exciting. In this review I examine what possible pathways we can take to understanding the controlling behavior of parasites and how host behavior has become an extended phenotype of the parasites that is often hidden from view. Host–parasite molecular cross-talk during the manipulative process of a host by its parasite Many parasite taxa are able to alter a wide range of phenotypic traits of their hosts in ways that seem to improve the parasite’s chance of completing its life cycle. Host behavioural alterations are classically seen as compelling illustrations of the ‘extended phenotype’ concept, which suggests that parasite genes have phenotype effects on the host. The molecular mechanisms and the host–parasite cross-talk involved during the manipulative process of a host by its parasite are still poorly understood. In this Review, the current knowledge on proximate mechanisms related to the ‘parasite manipulation hypothesis’ is presented. Parasite genome sequences do not themselves provide a full explanation of parasite biology nor of the molecular cross-talk involved in host–parasite associations. Recently, first-generation proteomics tools have been employed to unravel some aspects of the parasite manipulation process (i.e. proximate mechanisms and evolutionary convergence) using certain model arthropod-host–parasite associations. The pioneer proteomics results obtained on the manipulative process are here highlighted, along with the many gaps in our knowledge. Candidate genes and biochemical pathways potentially involved in the parasite manipulation are presented. Finally, taking into account the environmental factors, we suggest new avenues and approaches to further explore and understand the proximate mechanisms used by parasite species to alter phenotypic traits of their hosts.

Evolution of Multicellularity In Lab Yeast

Blasdelb — Fri, 09 Nov 2012 11:55:36 -0800

In just a few weeks single-celled yeast have evolved into a multicellular organism, complete with division of labour between cells. This suggests that the evolutionary leap to multicellularity may be a surprisingly small hurdle. More from Scientific American blogs. [Full Text PDF of the Publication of Note] More from the lab, with videos:

Snowflake reproduction 2:The snowflakes reproduce by spitting out "propagules" once they reach a large size. Once the propagule has grown (through a series of cell divisions) to be large enough, it too spits out a new propagule. Snowflake settling: The multicellular yeast clusters look like "snowflakes" as they settle to the bottom of their container. Snowflake genetic stability: Single cells of snowflake-phenotype yeast regenerate new snowflake-phenotype clusters. Snowflake size evolution: Time-lapse microscopy of derived rapid settling (left) and slow settling (right) genotypes isolated from 5 minute and 25 minute settling regimes, respectively. Cultures were grown for 24 h, diluted 300-fold, and grown in 0.5 uL YPD. Time-lapse microscopy was performed with images taken every minute for 600 minutes.

The actual paper is very accessibly written and totally understandable by the average non-creationist:

Experimental evolution of multicellularity (PDF) Multicellularity was one of the most significant innovations in the history of life, but its initial evolution remains poorly understood. Using experimental evolution, we show that key steps in this transition could have occurred quickly. We subjected the unicellular yeast Saccharomyces cerevisiae to an environment in which we expected multicellularity to be adaptive. We observed the rapid evolution of clustering genotypes that display a novel multicellular life history characterized by reproduction via multicellular propagules, a juvenile phase, and determinate growth. The multicellular clusters are uniclonal, minimizing within-cluster genetic conflicts of interest. Simple among-cell division of labor rapidly evolved. Early multicellular strains were composed of physiologically similar cells, but these subsequently evolved higher rates of programmed cell death (apoptosis), an adaptation that increases propagule production. These results show that key aspects of multicellular complexity, a subject of central importance to biology, can readily evolve from unicellular eukaryotes..

The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes.

Blasdelb — Mon, 22 Oct 2012 06:46:05 -0800

One of the many problems farmers of various kinds of legumes need to deal with is the pea aphid. They reproduce incredibly fast and live by sucking the sap out of the plants, an electron micrograph of one in action. However, while they are terrifying parasites of legumes, they have their own yet more horrific parasites, a parasitoid wasp. Here is a really nice close up picture of one doing its thing, a video of the act, and here is a brain meltingly horrific video of a dissection of the mummified aftermath 8 days later. Essentially, these wasps deposit their eggs in a pea aphid and the growing larva feeds on it, developing there for about a week, and then consuming the host from the inside out like a Xenomorph. When it’s done, the wasp larva dries the aphid’s cuticle into a papery brittle shell and an adult wasp emerges from the aphid mummy. Legume farmers love them, and you can even order their mummies online these days. However, farmers noticed that the wasps didn't work as effectively on all of the aphids, and so researchers went to work figuring out why. It turns out that all aphids have a primary bacterial endosymbiont living inside their cells, in addition to and just like a mitochondria, and that many have some combination of five other secondary endosymbionts. Interestingly, two of those other five, Hamiltonella defensa and Serratia symbiotica have been shown to confer varying levels of resistance to the parasitoid wasp, allowing the aphid to survive infection. However, it turns out that there is yet one more layer to this story, The relationship these endosymbionts have with the aphid, as well as the primary endosymbiont, is hard to classify as they confer a fitness cost in the absence of the wasp but a significant fitness boost when the wasps are around and trying to infect the aphids. At least for H. defensa, the reason why some strains are fully parasitic and provide no protection against the wasps while others are at least plausibly commensal and do provide protection, is a bacterial virus that infects the endosymbiont, even while it is inside the eukaryotic aphid cell. To understand why it will require a bit of knowledge of how some bacteriophages work. Most bacterial viruses, also known as bacteriophages, have a clear dividing line between two strategies. The simplest and most virulent phages will always immediately shut down their host’s metabolism upon infection and replace it with their own. Within a short period of time, generally between 20 and 80 minutes, the phage will have used the host cell to replicate its genome, build new viral particles, packed those particles with the genome and lysed the cell; setting loose 30-3000 new inert infectious particles. These are known as obligately lytic phages. Most phages however, use a mix of this strategy and another one known as lysogeny. These temperate phages will, at the beginning, decide to either virulently infect, producing particles at the total expense of the host, or hide in the host’s genome and inactivate all of its many host lethal genes. Generally it does this by expressing a transcriptional repressor that prevents expression of everything but the repressor, which incidentally protects the host from subsequent infection by related phages. However, some temperate phages will allow for expression of a genomic cassette that will perform some function of benefit to their host - they might as well since they are completely dependent on their host's wellbeing while in this stage of their life cycle. It turns out that there is a temperate bacteriophage called APSE, which is common in H. defensa populations in the aphids, that encodes for a cassette of genes that causes H. defensa to attack the wasp larvae with vicious toxins while the phage hides in the genome of its bacterial host. This makes for a really fascinatingly complex system of interdependencies for each of the agents involved. The phage, the bacterial symbiont, and the aphid are all each united in their interdependent need to combat the wasp that kills all three when it succeeds. However, at the same time, both the phage and the bacteria are dependent on the wasp to apply pressure on the aphid to keep them around - otherwise the aphid would cure itself of both creatures that would then be free-loading. Additionally, the wasp the bacteria, and the phage are all completely dependent on the aphid’s sap sucking ability to sustain them, and the aphid is totally dependent on the farmer to continue growing legumes in massive vulnerable monocultures. Furthermore the farmer and the legumes are dependent on the wasp to combat the aphid and largely helpless against the bacteria and the phage. At the same time, despite all of the interlocking incentives toward cooperation, there are also incentives towards each of these agents cheating each other. The farmer has an incentive to ‘cheat’ and save money by neglecting to buy aphid mummies every so often, because they still benefit from the fitness cost caused by the aphid not rejecting the bacteria or the bacteria rejecting the phage. Similarly, the aphid has an incentive to cheat both the bacteria and the phage to cure itself of them and bet on the farmer not buying aphid mummies full of wasps that year. The bacteria also has an incentive to cheat the aphid by curing itself of the phage, and also bet on the farmer not buying mummies that year itself. Oliver KM, Degnan PH, Hunter MS, & Moran NA. 2009. Bacteriophages encode factors required for protection in a symbiotic mutualism. Science 325(5943); 992-4. [REQUIRES FREE REGISTRATION]

Bacteriophages are known to carry key virulence factors for pathogenic bacteria, but their roles in symbiotic bacteria are less well understood. The heritable symbiont Hamiltonella defensa protects the aphid Acyrthosiphon pisum from attack by the parasitoid Aphidius ervi by killing developing wasp larvae. In a controlled genetic background, we show that a toxin-encoding bacteriophage is required to produce the protective phenotype. Phage loss occurs repeatedly in laboratory-held H. defensa–infected aphid clonal lines, resulting in increased susceptibility to parasitism in each instance. Our results show that these mobile genetic elements can endow a bacterial symbiont with benefits that extend to the animal host. Thus, phages vector ecologically important traits, such as defense against parasitoids, within and among symbiont and animal host lineages.

Moran NA, Degnan PH, Santos SR, Dunbar HE, & Ochman H. 2005. The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes. PNAS USA, 102(47); 16919-26.

Aphids maintain mutualistic symbioses involving consortia of coinherited organisms. All possess a primary endosymbiont, Buchnera, which compensates for dietary deficiencies; many also contain secondary symbionts, such as Hamiltonella defensa, which confers defense against natural enemies. Genome sequences of uncultivable secondary symbionts have been refractory to analysis due to the difficulties of isolating adequate DNA samples. By amplifying DNA from hemolymph of infected pea aphids, we obtained a set of genomic sequences of H. defensa and an associated bacteriophage. H. defensa harbors two type III secretion systems, related to those that mediate host cell entry by enteric pathogens. The phage, called APSE-2, is a close relative of the previously sequenced APSE-1 but contains intact homologs of the gene encoding cytolethal distending toxin (cdtB), which interrupts the eukaryotic cell cycle and which is known from a variety of mammalian pathogens. The cdtB homolog is highly expressed, and its genomic position corresponds to that of a homolog of stx (encoding Shiga-toxin) within APSE-1. APSE-2 genomes were consistently abundant in infected pea aphids, and related phages were found in all tested isolates of H. defensa, from numerous insect species. Based on their ubiquity and abundance, these phages appear to be an obligate component of the H. defensa life cycle. We propose that, in these mutualistic symbionts, phage-borne toxin genes provide defense to the aphid host and are a basis for the observed protection against eukaryotic parasites.

This post is deeply endebted to one made on Moselio Schaechter's blog Small Things Considered, which is no doubt more clearly written.

Virulence-transmission trade-offs and population divergence in virulence

Blasdelb — Sun, 21 Oct 2012 04:35:01 -0800

"Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking." Two papers demonstrate empirical evidence for related models predicting the origin of virulence: de Roode JC, Yates AJ, & Altizer S. 2007. Timing of transmission and the evolution of virulence of an insect virus. Proc. R. Soc. Lond. B 269(1496); 1161-1165.

We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts. [Full Text HTML] [Full Text PDF]

Cooper VS, Reiskind MH, Miller JA, Shelton KA, Walther BA, Elkinton JS, & Ewald PW. 2002. Virulence-transmission trade-offs and population divergence in virulence in a naturally occurring butterfly parasite (PDF). PNAS 105(21); 7489-7494.

Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking. We studied a protozoan parasite of monarch butterflies and found that higher levels of within-host replication resulted in both higher virulence and greater transmission, thus lending support to the idea that selection for parasite transmission can favor parasite genotypes that cause substantial harm. Parasite fitness was maximized at an intermediate level of parasite replication, beyond which the cost of increased host mortality outweighed the benefit of increased transmission. A separate experiment confirmed genetic relationships between parasite replication and virulence, and showed that parasite genotypes from two monarch populations caused different virulence. These results show that selection on parasite transmission can explain why parasites harm their hosts, and suggest that constraints imposed by host ecology can lead to population divergence in parasite virulence. [Abstract HTML] [Full Text PDF]

The Puzzle of Plastid Evolution

Blasdelb — Sat, 20 Oct 2012 04:13:36 -0800

The Puzzle of Plastid Evolution: A comprehensive understanding of the origin and spread of plastids remains an important yet elusive goal in the field of eukaryotic evolution. Combined with the discovery of new photosynthetic and non-photosynthetic protist lineages, the results of recent taxonomically broad phylogenomic studies suggest that a re-shuffling of higher-level eukaryote systematics is in order. Consequently, new models of plastid evolution involving ancient secondary and tertiary endosymbioses are needed to explain the full spectrum of photosynthetic eukaryotes. [Full Text HTML] [Full Text PDF] Our planet is teeming with photosynthetic life. The textbook version of how this came to be is relatively straightforward: oxygenic photosynthesis first evolved in the ancestors of modern cyanobacteria more than two billion years ago [1] and their light-harvesting capabilities were subsequently exploited by eukaryotic (nucleus-containing) cells through the process of endosymbiosis [2 PDF] and [3 PDF]. Co-evolving with their opportunistic hosts, these intracellular cyanobacteria were eventually transformed into bona fide organelles — plastids — ultimately giving rise to the plants and algae that surround us today. Easy, right? The basic outline of this evolutionary scenario is correct, but the reality is much, much more complicated. Photosynthetic eukaryotes are astonishingly diverse in form and function, a fact that complicates efforts to discern their evolutionary history. Eukaryotic phototrophs can be macroscopic (e.g., land plants, seaweed) or microscopic (e.g., the unicellular green alga Chlamydomonas), sessile or motile (or both), and given a bit of sunlight, they thrive in virtually any habitat imaginable, terrestrial and aquatic, from the equator to the poles. This vast diversity actually makes sense when one considers that the term ‘algae’ can be applied to organisms that are not specifically related to one another. In addition to simple vertical inheritance, plastids have on multiple occasions spread laterally between distantly related groups of eukaryotes. Having evolved ∼one billion years in the past [4], today's plastids weave a tangled web across a very large fraction of the eukaryotic tree. Consequently, large sections of the puzzle of plastid evolution remain unassembled. This article focuses on the latest advances in our understanding of the origin and spread of plastids. In particular, the merits and shortcomings of competing hypotheses about the evolution of plastids are discussed in light of a flood of new molecular, biochemical, genomic and phylogenomic data. Progress has been swift, but there are still many questions that need to be answered, and many newly discovered protist lineages that need to be investigated, before it can be said that the evolution of eukaryotic photosynthesis is understood with confidence. Don't miss the very pretty trees.

Mitigating Mutational Meltdown in Mammalian Mitochondria

Blasdelb — Fri, 19 Oct 2012 03:21:08 -0800

Mitigating Mutational Meltdown in Mammalian Mitochondria PLoS Biol 6(2): e35. [The PDF, where you can read the paper in its much prettier intended format.]

Mitochondria are remarkable microorganisms. About two billion years ago, their distant free-living ancestors hooked up with a truly foreign lineage of archaebacteria and started a genomic merger that led to the most successful coevolved mutualism on the planet: the eukaryotic cell. Along the way, evolving mitochondria lost a lot of genomic baggage, entrusted their emerging hosts with their own replication, sorted out genomic conflicts by following maternal inheritance, and have mostly abstained from sex and recombination. What mitochondria did retain was a subset of genes that encode critical components of the electron transport chain and ATP synthesis enzymes that carry out oxidative phosphorylation. Because mitochondria house the biochemical machinery that requires us to breathe oxygen, it was first assumed that mitochondrial genes would show very slow rates of molecular evolution. So it was big news almost 30 years ago when mitochondrial DNA (mtDNA) evolution was observed to be quite rapid ^[1]. How could the genes for a highly conserved and critical function sustain the consequences of high mutation pressure and permit rapid rates of nucleotide substitution between species? Without the benefits of recombination, where offspring can carry fewer mutations than either parent, mutations should accumulate in mitochondrial genomes through the random loss of less-mutated genomes, a process referred to as Muller's ratchet ^[2,3]. How have mitochondria avoided a mutational meltdown, or at least significant declines in fitness?

Here is a jaw droppingly beautiful 3D animation of what Mitochindria look like in action. A quick explanation of Muller's Ratchet by MetaFilter's own Scientist

Constitutive formation of caveolae in a bacterium.

Blasdelb — Thu, 18 Oct 2012 02:55:45 -0800

Constitutive formation of caveolae in a bacterium. [Full Text]

Caveolin plays an essential role in the formation of characteristic surface pits, caveolae, which cover the surface of many animal cells. The fundamental principles of caveola formation are only slowly emerging. Here we show that caveolin expression in a prokaryotic host lacking any intracellular membrane system drives the formation of cytoplasmic vesicles containing polymeric caveolin. Vesicle formation is induced by expression of wild-type caveolins, but not caveolin mutants defective in caveola formation in mammalian systems. In addition, cryoelectron tomography shows that the induced membrane domains are equivalent in size and caveolin density to native caveolae and reveals a possible polyhedral arrangement of caveolin oligomers. The caveolin-induced vesicles or heterologous caveolae (h-caveolae) form by budding in from the cytoplasmic membrane, generating a membrane domain with distinct lipid composition. Periplasmic solutes are encapsulated in the budding h-caveola, and purified h-caveolae can be tailored to be targeted to specific cells of interest.

Elio Schaechter writes in plain English about how fantastically amazing and unexpected the researchers actually pulling this off is, and he also talks about it in more detail in his podcast.

Provirophages and transpovirons as the diverse mobilome of giant viruses

Blasdelb — Tue, 16 Oct 2012 15:55:54 -0800

Provirophages and transpovirons as the diverse mobilome of giant viruses

Abstract: A distinct class of infectious agents, the virophages¹ that infect giant viruses of the Mimiviridae family, has been recently described. Here we report the simultaneous discovery of a giant virus of Acanthamoeba polyphaga (Lentille virus) that contains an integrated genome² of a virophage (Sputnik 2), and a member of a previously unknown class of mobile genetic elements³, the transpovirons⁴. The transpovirons are linear DNA elements of ∼7 kb [kilobases]⁵ that encompass six to eight protein-coding genes, two of which are homologous⁶ to virophage genes. Fluorescence⁷ in situ hybridization⁸ showed that the free form of the transpoviron replicates within the giant virus factory and accumulates in high copy numbers inside giant virus particles, Sputnik 2 particles, and amoeba cytoplasm. Analysis of deep-sequencing data showed that the virophage and the transpoviron can integrate⁹ in nearly any place in the chromosome of the giant virus host and that, although less frequently, the transpoviron can also be linked to the virophage chromosome. In addition, integrated fragments of transpoviron DNA were detected in several giant virus and Sputnik genomes. Analysis of 19 Mimivirus strains revealed three distinct transpovirons associated with three subgroups of Mimiviruses. The virophage, the transpoviron, and the previously identified self-splicing introns¹⁰ and inteins¹¹ constitute the complex, interconnected mobilome¹² of the giant viruses and are likely to substantially contribute to interviral gene transfer.

[Full Text PDF] and two explanations in English (*#*) indicates that the article referenced is openly accessible Introduction:

Mobile genetic elements (MGEs) that are collectively referred to as the “mobilome” are key players in the genome evolution of prokaryotes (*1*) and eukaryotes (*2*, *3*) and are considered “genetic engineers” of biological innovation (*1*). MGEs can be roughly grouped into four major classes: transposable elements (TEs), plasmids, viruses, and self-splicing elements such as group I and II introns and inteins (*4*). The mobilomes of many bacteria, archaea, and unicellular eukaryotes include all of these elements in a free or integrated form. Given that viruses constitute a part of the mobilome, they are not normally considered to possess mobilomes of their own. However, some large viruses contain retrovirus sequences integrated into their genomes (*5*, *6*), whereas others, including members of the Mimiviridae family, harbor self-splicing introns and/or inteins (*7*, *8*, *9*). Furthermore, many viruses support the reproduction of satellite viruses¹ (*10*). The discovery of the Sputnik virophage in 2008 added a new twist to the existing understanding of the relationships between different mobile elements by demonstrating for the ﬁrst time that a giant virus could be infected by another, much smaller virus in a manner similar to the viral infection of cells (11). The Sputnik virophage is a small icosahedral virus (74 nm in diameter) that parasitizes on Mamavirus, a member of the Mimiviridae family (12, 13). Sputnik replicates inside Mamavirus or Mimivirus viral factories when the host giant virus is grown in amoebae such as Acanthamoeba castellanii or A. polyphaga (11). An in-depth analysis of the Sputnik proteins has suggested an evolutionary connection between this virophage and a distinct class of TEs (14). The second virophage, the Mavirus (15), was isolated as a parasite of a distinct member of the Mimiviridae family, Cafeteria roenbergensis virus (CroV) [Previously on Metafilter] (16). At least four Mavirus proteins, including the major capsid protein¹³, are homologous⁶ to proteins of Sputnik. In addition, the Mavirus genome encodes a retroviral-type integrase and a protein-primed DNA polymerase B; these proteins are homologous to the respective proteins of Maverick/polinton DNA transposons, which insert into genomes of diverse eukaryotes, suggesting an evolutionary link between the Mavirus and the polintons (15). The third complete virophage genome sequence has been identiﬁed in the metagenome of the hypersaline Organic Lake in Antarctica (*17*). This Organic Lake virophage (OLV) is thought to parasitize on phycoDNAviruses that infect green algae. The OLV genome encodes seven proteins with homologs in Sputnik (*17*), including two key proteins, the major capsid protein and the DNA-packaging ATPase, that are shared by all three virophages. Thus, the virophages apparently share a common origin, although each underwent multiple gene replacements. The virophages are likely to be common parasites of nucleocytoplasmic large DNA viruses that infect diverse eukaryotes, and show multiple evolutionary connections to other mobile elements (*18*). Here we present ﬁndings that substantially expand the complexity of the giant virus mobilome through the description of an integrated form of the virophage and of a distinct class of MGEs, the transposovirons.

Discussion:

The discovery of the Mimivirus and subsequent identiﬁcation of other giant viruses revealed unexpected complexity of viral genomes that, with over 1,000 protein-coding genes, are more complex than many parasitic and symbiotic bacteria and are comparable to the most compact genomes of free-living bacteria and archaea (*7*). The present work shows that giant viruses are associated with a commensurately complex mobilome that encompasses three of the four major classes of mobile elements, namely self-splicing elements, transposable elements or linear plasmids (transpovirons), and viruses (virophages that can form provirophages after integration into the host giant virus genome). Different components of the giant virus mobilome share homologous genes, and genomic comparisons point to DNA transfer between the mobilome components and the host virus but also within the mobilome itself. Thus, the giant virus mobilome is a network that potentially could provide routes and vehicles for gene exchange and might make substantial contributions to the shaping of mosaic viral genomes. The giant viruses and their mobilomes together are part of even more expansive, dynamic genetic networks: the amoebae with their diverse bacterial parasites and symbionts and their own viruses (30). Of special note is the transpoviron, a distinct plasmid that depends on giant viruses for its replication and spread. Substantial analogies can be found between the transpovirons and virus-associated plasmids present in bacteria and archaea. In particular, the well-studied bacteriophage P4 (also known as a “phasmid”) is a plasmid that replicates episomally in the absence of the helper bacteriophage P2 but is encapsidated into virions and thus can infect new bacterial cells in the presence of the helper (*31*, *32*). A similar replication strategy has been described for the archaeal virus plasmid pSSVx that depends on the fuselloviruses SSV1 or SSV2 and appears to have acquired genes from a fusellovirus (33). The discovery of the transpoviron shows that virus-associated plasmids exist in all three domains of cellular life. It is unlikely that the present study exhausts the diversity of the giant virus mobilome; additional virophages and transpovirons, and perhaps distinct classes of mobile elements, are likely to be discovered. Indeed, the transpoviron had not been detected until the isolation of Lentille virus from a human sample described here. Furthermore, we failed to detect closely related homologs of transpoviron genes in the available databases of environmental sequences, although close homologs of many Mimivirus and Sputnik genes were readily detectable (11). Thus, speciﬁc conditions and/or habitats could be required for accumulation of transpovirons and probably other elements comprising the giant virus mobilome. Characterization of such conditions will likely lead to the discovery of additional genetic elements associated with giant viruses and facilitate elucidation of their replication mechanisms and the relationships between different mobilome components.

Glossary of Terms Used in the Abstract, Introduction, and Discussion:

¹Virophage: A subviral agent composed of nucleic acid that depends on the co-infection of a host cell with a helper or master virus for its multiplication. When a satellite encodes the coat protein in which its nucleic acid is encapsidated it is referred to as a satellite virus. A satellite virus of mimivirus that inhibits the replication of its host has been termed a virophage. However, the usage of this term remains controversial due to the lack of fundamental differences between virophages and classical satellite viruses. ²Integrated Genome: A prophage is a phage (viral) genome inserted and integrated into the circular bacterial DNA chromosome. A prophage, also known as a temperate phage, is any virus in the lysogenic cycle; it is integrated into the host chromosome or exists as an extrachromosomal plasmid. Technically, a virus may be called a prophage only while the viral DNA remains incorporated in the host DNA. This is a latent form of a bacteriophage, in which the viral genes are incorporated into the bacterial chromosome without causing disruption of the bacterial cell. Upon detection of host cell damage, such as UV light or certain chemicals, the prophage is excised from the bacterial chromosome in a process called prophage induction. After induction, viral replication begins via the lytic cycle. In the lytic cycle, the virus commandeers the cell's reproductive machinery. The cell may fill with new viruses until it lyses or bursts, or it may release the new viruses one at a time in a reverse endocytotic process. The period from infection to lysis is termed the latent period. A virus following a lytic cycle is called a virulent virus. Prophages are important agents of horizontal gene transfer, and are considered part of the mobilome. ³Mobile genetic elements: Mobile genetic elements (MGE) are a type of DNA that can move around within the genome. They include Transposons (also called transposable elements including Retrotransposons, DNA transposons, and Insertion sequences), Plasmids, Bacteriophage elements like Mu (which integrates randomly into the genome), and Group II introns. The total of all mobile genetic elements in a genome may be referred to as the mobilome. ⁴Transpoviron: This is a new term that the authors are proposing to refer to mobile genetic elements within viruses. ⁵Kb or Kilobasepairs: A measurement of the length of a stretch of DNA equivalent to 1,000 base pairs ⁶Homology: Homologous traits of organisms are due to sharing a common ancestor, and such traits often have similar embryological origins and development. This is contrasted with analogous traits: similarities between organisms that were not present in the last common ancestor of the taxa being considered but rather evolved separately. An example of analogous traits would be the wings of bats and birds, which evolved separately but both of which evolved from the vertebrate forelimb and therefore have similar early embryology. Whether or not a trait is homologous depends on both the taxonomic and anatomical levels at which the trait is examined. For example, the bird and bat wings are homologous as forearms in tetrapods. However, they are not homologous as wings, because the organ served as a forearm (not a wing) in the last common ancestor of tetrapods. By definition, any homologous trait defines a clade—a monophyletic taxon in which all the members have the trait (or have lost it secondarily); and all non-members lack it ⁷Fluorescence: The emission of light by a substance that has absorbed light or other electromagnetic radiation. It is a form of luminescence. In most cases, the emitted light has a longer wavelength, and therefore lower energy, than the absorbed radiation. However, when the absorbed electromagnetic radiation is intense, it is possible for one electron to absorb two photons; this two-photon absorption can lead to emission of radiation having a shorter wavelength than the absorbed radiation. The emitted radiation may also be of the same wavelength as the absorbed radiation, termed "resonance fluorescence". ⁸In situ hybridization: A type of hybridization that uses a labeled complementary DNA or RNA strand (i.e., probe) to localize a specific DNA or RNA sequence in a portion or section of tissue (in situ) ⁹Viral Integration: A superpower possessed by Eukaryotic retroviruses (like HIV and Human T-lymphotropic virus) and temperate bacteriophages, where the virus integrates its genome into its host's genome and shuts off ll of its host lethal genes in order to hide - indefinitely - until conditions become better for an active infection. ¹⁰Intron: An intron is any nucleotide sequence within a gene that is removed by RNA splicing while the final mature RNA product of a gene is being generated. The term intron refers to both the DNA sequence within a gene, and the corresponding sequence in RNA transcripts. Sequences that are joined together in the final mature RNA after RNA splicing are exons. Introns are found in the genes of most organisms and many viruses, and can be located in a wide range of genes, including those that generate proteins, ribosomal RNA (rRNA), and transfer RNA (tRNA). When proteins are generated from intron-containing genes, RNA splicing takes place as part of the RNA processing pathway that follows transcription and precedes translation. The word intron is derived from the term intragenic region; i.e., a region inside a gene. Although introns are sometimes called intervening sequences, the term "intervening sequence" can refer to any of several families of internal nucleic acid sequences that are not present in the final gene product, including inteins, untranslated sequences (UTR), and nucleotides removed by RNA editing, in addition to introns. ¹¹Intein: An intein is a segment of a protein that is able to excise itself and rejoin the remaining portions (the exteins) with a peptide bond. Inteins have also been called "protein introns". ¹²Mobilome: The total of all mobile genetic elements in a genome; a play on the word Genome. ¹³Major Capsid Protein: A capsid is the protein shell of a virus. It consists of several oligomeric structural subunits made of protein called protomers. The observable 3-dimensional morphological subunits, which may or may not correspond to individual proteins, are called capsomeres. The capsid encloses the genetic material of the virus.

References from the Introduction and Discussion:

1. Frost LS, Leplae R, Summers AO, Toussaint A (2005) Mobile genetic elements: The agents of open source evolution. Nat Rev Microbiol 3(9):722–732. 2. Feschotte C, Pritham EJ (2007) DNA transposons and the evolution of eukaryotic genomes. Annu Rev Genet 41:331–368. 3. Kazazian HH, Jr. (2004) Mobile elements: Drivers of genome evolution. Science 303 (5664):1626–1632. 4. Siefert JL (2009) Defining the mobilome. Methods Mol Biol 532:13–27. 5. Sun AJ, et al. (2010) Functional evaluation of the role of reticuloendotheliosis virus long terminal repeat (LTR) integrated into the genome of a field strain of Marek’s disease virus. Virology 397(2):270–276. 6. Hertig C, Coupar BEH, Gould AR, Boyle DB (1997) Field and vaccine strains of fowlpox virus carry integrated sequences from the avian retrovirus, reticuloendotheliosis virus. Virology 235(2):367–376. 7. Raoult D, et al. (2004) The 1.2-megabase genome sequence of Mimivirus. Science 306 (5700):1344–1350. 8. Colson P, et al. (2011) Viruses with more than 1,000 genes: Mamavirus, a new Acanthamoeba polyphaga mimivirus strain, and reannotation of Mimivirus genes. Genome Biol Evol 3:737–742. 9. Van Etten JL (2003) Unusual life style of giant chlorella viruses. Annu Rev Genet 37: 153–195. 10. Simon AE, Roossinck MJ, Havelda Z (2004) Plant virus satellite and defective interfering RNAs: New paradigms for a new century. Annu Rev Phytopathol 42: 415–437. 11. La Scola B, et al. (2008) The virophage as a unique parasite of the giant mimivirus. Nature 455(7209):100–104. 12. Sun S, et al. (2010) Structural studies of the Sputnik virophage. J Virol 84(2):894–897. 13. Desnues C, Raoult D (2010) Inside the lifestyle of the virophage. Intervirology 53(5): 293–303. 14. Iyer LM, Abhiman S, Aravind L (2008) A new family of polymerases related to superfamily A DNA polymerases and T7-like DNA-dependent RNA polymerases. Biol Direct 3:39. 15. Fischer MG, Suttle CA (2011) A virophage at the origin of large DNA transposons. Science 332(6026):231–234. 16. Fischer MG, Allen MJ, Wilson WH, Suttle CA (2010) Giant virus with a remarkable complement of genes infects marine zooplankton. Proc Natl Acad Sci USA 107(45): 19508–19513. 17. Yau S, et al. (2011) Virophage control of Antarctic algal host-virus dynamics. Proc Natl Acad Sci USA 108(15):6163–6168. 18. Koonin EV, Yutin N (2010) Origin and evolution of eukaryotic large nucleo-cytoplasmic DNA viruses. Intervirology 53(5):284–292. 30. Raoult D, Boyer M (2010) Amoebae as genitors and reservoirs of giant viruses. In- tervirology 53(5):321–329. 31. Briani F, Dehò G, Forti F, Ghisotti D (2001) The plasmid status of satellite bacterio- phage P4. Plasmid 45(1):1–17. 32. Lindqvist BH, Dehò G, Calendar R (1993) Mechanisms of genome propagation and helper exploitation by satellite phage P4. Microbiol Rev 57(3):683–702. 33. Arnold HP, et al. (1999) The genetic element pSSVx of the extremely thermophilic crenarchaeon Sulfolobus is a hybrid between a plasmid and a virus. Mol Microbiol 34 (2):217–226.

Bonus:

Carl Zimmer's explanation of the debate over whether these Nucleocytoplasmic Large DNA Viruses (Giant) viruses constitute a new fourth domain of life.

Pertussis Epidemic — Washington, 2012

Blasdelb — Thu, 27 Sep 2012 03:08:08 -0800

Since mid-2011, a substantial rise in pertussis [Whooping Cough] cases has been reported in the state of Washington. In response to this increase, the Washington State Secretary of Health declared a pertussis epidemic on April 3, 2012. By June 16, the reported number of cases in Washington in 2012 had reached 2,520 (37.5 cases per 100,000 residents), a 1,300% increase compared with the same period in 2011 and the highest number of cases reported in any year since 1942 [Make sure you don't miss Figure 1]. Commentators are already drawing corellations with the fact that Washington State leads the nation in vaccine non-compliance, Washington State's recent cutbacks in public health funding, and increases in the number of uninsured (PDF). Valid vaccination history was available for 1,829 of 2,006 (91.2%) patients aged 3 months–19 years. Overall, 758 of 1,000 (75.8%) patients aged 3 months–10 years were up-to-date with the childhood diphtheria and tetanus toxoids and acellular pertussis (DTaP) doses. Receipt of Tdap was documented in 97 of 225 (43.1%) patients aged 11–12 years and in 466 of 604 (77.2%) patients aged 13–19 years. Estimated DTaP coverage in Washington among children aged 19–35 months was 93.2% for ≥3 doses and 81.9% for ≥4 doses in 2010; Tdap coverage in adolescents aged 13–17 years was estimated at 70.6%* This means that while vaccination still provides individual protection - with unvaccinated children being eight times more likely to get whooping cough and, when they do, become more infectious, have stronger symptoms, are sick longer and are at greater risk of severe outcomes, including hospitalization - communal failures to vaccinate have allowed gaps in herd immunity to expose vaccinated children to more pertussis than the vaccine can provide absolute protection against while also simultaneously breeding vaccine resistant strains. Here is disturbing footage of what pertussis looks like in 12 week old and 6 month old babies, as well as various children, whooping cough is back.

There are fewer microbes out there than you think

Blasdelb — Tue, 28 Aug 2012 09:01:36 -0800

There are fewer microbes out there than you think. New estimate reduces the number of microbes on Earth by around half. Current consensus: Kallmeyera J, Pockalnyc R, Adhikaria RR, Smith DC, & D’Hondtc S. 2012. Global distribution of microbial abundance and biomass in subseafloor sediment. in press - doi: 10.1073/pnas.1203849109. [ABSTRACT] [FULL TEXT PDF] Previous consensus: Whitman WB,Coleman DC, & Wiebe WJ. 1998. Prokaryotes: The unseen majority. PNAS 95(12): 6578-6583 [FULL TEXT HTML] [FULL TEXT PDF] Related: Slo-mo microbes extend the frontiers of life Community in the deep seabed uses so little oxygen that it is no longer clear where the lower bound for life lies. Geomicrobiology: Low life The boundaries of biology reach farther below Earth's surface than scientists had thought possible. Amanda Leigh Mascarelli delves into how microbes survive deep underground.

Chagas Disease: Poverty, Immigration, and the ‘New HIV/AIDS’

Blasdelb — Wed, 30 May 2012 15:26:47 -0800

What if a deadly epidemic was burgeoning and almost nobody noticed? In the latest issue of PLoS Neglected Tropical Diseases, a distinguished group of virologists, epidemiologists and infectious-disease specialists say that’s not a hypothetical question. They argue that Chagas disease, a parasitic infection transmitted by blood-sucking insects, has become so widespread and serious — while remaining largely unrecognized — that it deserves to be considered a public health emergency. Extending the metaphor, they liken Chagas’ stealth spread to the early days of AIDS:
"Both diseases are health disparities, disproportionately affecting people living in poverty. Both are chronic conditions requiring prolonged treatment courses… As with patients in the first two decades of the HIV/AIDS epidemic, most patients with Chagas disease do not have access to health care facilities. Both diseases are also highly stigmatizing, a feature that for Chagas disease further complicates access to … essential medicines, as well as access to serodiagnosis and medical counseling."
Hotez PJ, Dumonteil E, Woc-Colburn L, et al. (2012) Chagas Disease: “The New HIV/AIDS of the Americas”. PLoS Negl Trop Dis 6(5): e1498. doi:10.1371/journal.pntd.0001498 Tanowitz HB, Weiss LM, Montgomery SP (2011) Chagas Disease Has Now Gone Global. PLoS Negl Trop Dis 5(4): e1136. doi:10.1371/journal.pntd.0001136 Sarkar S, Strutz SE, Frank DM, et al. (2010) Chagas Disease Risk in Texas. PLoS Negl Trop Dis 4(10): e836. doi:10.1371/journal.pntd.0000836

0.0001 micromoles of oxygen per liter per year

jjray — Sat, 19 May 2012 19:38:49 -0800

If we look at how fast they metabolize, it would take them a thousand years just to reproduce themselves. They may be much older than this. There’s no way of knowing.

Microbes found deep under the North Pacific Gyre in 86-million-year-old red clay, potentially millions of years old, force us to rethink the timescales, ranges, and conditions that life can attain. (The main text of the paper is unfortunately paywalled.)

How Corporations Corrupt Science at the Public's Expense

Blasdelb — Sun, 11 Mar 2012 11:17:54 -0800

How Corporations Corrupt Science at the Public's Expense: Report looks at methods of corporate abuse, suggests steps toward reform [Full Report (PDF)] [Executive Summary (PDF)] The report includes telling examples of Suppressing Research,

a USDA microbiologist was prevented from publishing research showing that emissions from industrial hog farms contained antibiotic-resistant bacteria

Dr. Ingacio Chapela of the University of California–Berkeley and graduate student David Quist published an article in Nature showing that DNA from genetically modified corn was contaminating native Mexican corn. The research spurred immediate backlash. Nature received a number of letters to the editor, including several comments on the Internet from "Mary Murphy" and "Andura Smetacek" accusing the scientists of bias. The backlash prompted Nature to publish an editorial agreeing that the report should not have been published. However, investigators eventually discovered that the comments from Murphy and Smetacek originated with The Bivings Group, a public relations firm that specializes in online communications and had worked for Monstanto. Mary Murphy and Andura Smetacek were found to be fictional names.

"Boots commissioned Dr. Betty Dong, a scientist at the University of California–San Francisco, to test the effects of Synthroid, a replacement for thyroid hormone. Boots hoped to reveal that despite its high price, Synthroid was more effective than similar drugs. The company closely monitored the research, and when Dong found that the drug was no more effective than its competitors, instructed her not to publish the results. When she refused to comply, Boots threatened to sue. The company relented only after several years, during which consumers continued to pay for the costly product."

Corrupting Advisory Panels:

"A few weeks before a CDC advisory panel met to discuss revising federal lead standards, two scientists with ties to the lead industry were added to the panel. The committee voted against tightening the standards."

"ReGen Biologics attempted to gain FDA approval for clinical trials of Menaflex, a device it developed to replace knee cartilage. After an FDA panel rejected the device, the company enlisted four members of Congress from its home state of New Jersey to influence the evaluation process. In December 2007, Senator Frank Lautenberg, Senator Robert Menendez, and Representative Steve Rothman wrote to FDA Commissioner Andrew von Eschenbach asking him to personally look into Menaflex. Soon thereafter, the commissioner met with ReGen executives and heeded the company's advice to have Dr. Daniel Shultz, head of the FDA's medical devices division, oversee a new review. The FDA fast-tracked and approved the product despite serious concerns from the scientific community."

Ghostwriting Articles:

"A 2011 analysis found evidence of corporate authorship in research articles on a variety of drugs, including Avandia, Paxil, Tylenol, and Vioxx."

"From 1998 to 2007, Pfizer discreetly facilitated the publication of 15 case studies, six case reports, and nine letters to the editor to boost off-label use of Neurontin, a drug prescribed to treat seizures in people who have epilepsy and nerve pain. The number of patients taking the drug rose from 430,000 to 6 million, making it one of Pfizer's most profitable products. An investigation found that Pfizer had failed to publish negative results, selectively reported outcomes, and excluded specific patients from analysis. [Most importantly] Pfizer failed to note that the drug increased the risk of suicide.'

Purchasing Rigged Research

'To counter a study that found that formaldehyde caused cancer in rats, a formaldehyde company commissioned its own study. That study-which found no association between the chemical and cancer-exposed only one-third the number of rats to formaldehyde for half as long as the original study. A formaldehyde association quickly publicized the results and argued before the Consumer Product Safety Commission (CPSC) that they indicated "no chronic health effects from exposure to the level of formaldehyde normally encountered in the home""

Creating Front Organizations

The Center for Consumer Freedom is a nonprofit that targets dietary guidelines recommended by the FDA, other government agencies, medical associations, and consumer advocacy organizations. The center has run ads and owns a website that accuses government agencies of overregulation, and has published articles claiming to refute evidence that high salt intake and other dietary guidelines are based on inadequate science. The center was founded with a $600,000 grant from Philip Morris, but has also received funding from Cargill, National Steak and Poultry, Monsanto, Coca-Cola, and Sutter Home Winery.

Purchasing Support from Existing Organizations

In 2003, the American Academy of Pediatric Dentistry accepted a $1 million donation from Coca-Cola. That year, the group claimed that "scientific evidence is certainly not clear on the exact role that soft drinks play in terms of children's oral disease." The statement directly contradicted the group's previous stance that "consumption of sugars in any beverage can be a significant factor…that contributes to the initiation and progression of dental caries."

The relentlessness of the simplest eukarya.

nicolas léonard sadi carnot — Tue, 31 Jan 2012 05:30:51 -0800

Gorgeous microphotography of the growth of colonial fungi species. Featuring aspergillus, fumigatus, botrytis, trichoderma, and cladosporidium.

Bioshock

Artw — Fri, 30 Sep 2011 15:37:10 -0800

Scientist and Science Fiction author Joan Slonczewski, author of A Door Into The Ocean, guest blogs about science fictional and microbiology on Charles Stross's site: Salt Beings, Microbes grow the starship, Synthetic Babies