The selfish gene is one of the most successful science metaphors ever invented. Unfortunately, it’s wrong.
X inactivation is a type of gene dosage compensation. In humans, the sex chromosomes X and Y determine the sex of an individual - females have two X chromosomes (XX), males have one X and one Y chromosome (XY). All of the genes on the Y chromosome are required in male development, while the genes on the X chromosome are needed for both male and female development. Because females receive two X chromosomes, they inherit two copies of many of the genes that are needed for normal function. Extra copies of genes or chromosomes can affect normal development. An example is Down's syndrome, which is caused by an extra copy of part or all of chromosome 21. In female mammals, a process called X inactivation has evolved to compensate for the extra X chromosome. In X inactivation, each cell 'switches off' one of its X chromosomes, chosen at random, to ensure the correct number of genes are expressed, and to prevent abnormal development.
Here is a helpful eleven minute description of what it is and why it's important by Etsuko Uno and metafilter's own Drew Berry in a fucking gorgeous Goodsell-esque 3D animation.[more inside]
What we currently call breast cancer should be thought of as 10 completely separate diseases, according to an international study which has been described as a "landmark". The categories could improve treatment by tailoring drugs for a patient's exact type of breast cancer and help predict survival more accurately. The study in Nature analysed breast cancers from 2,000 women [Abstract] . It will take at least three years for the findings to be used in hospitals. [more inside]
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.