On the Weizmann Wave, researchers have made a discovery surrounding exons—”bits of genetic code that are snipped out of the sequence and spliced together to make the protein instruction list.” When a cell needs to make a protein, it pulls exons out of pre-messenger RNA and stitches them together to form messenger RNA. Alternating sequences called introns are left out. By tracking the unused introns, researchers observed that “in some cases, pre-mRNA production shot straight up – to ten times or more than that of the mRNA that followed.” They call this “production overshoot,” for when “the cell needs a rush job on the manufacture of certain proteins.” On Pharyngula, PZ Myers tackles the phylogeny of modern primates. Although chimpanzees are our closest living relatives, 30% of the newly-sequenced gorilla genome is closer than chimp to human. This is the result of Independent Lineage Sorting, which Myers calls an expected outcome of evolution, not an obstacle to its acceptance. Myers says “The only way you would fail to see ILS is if every genetic difference between two species emerged simultaneously, in lockstep, in one grand swoop.” Like mRNA production, speciation in practice is a lot more messy.
We’ve all heard of bird and swine flu, but bats, which comprise “about a fifth of all known mammalian species,” also carry a diverse host of viruses. By swabbing the rectums of little yellow-shouldered bats, researchers in Guatemala discovered a new influenza virus that defies easy classification. Flu viruses are described by two key genes—hence the name ‘H1N1.’ Tara C. Smith writes “The novel bat virus was a completely new H type—type 17 (provisional, they note, pending further analyses). The NA gene was also highly divergent.” Smith continues “the authors did do some molecular work suggesting that these novel bat viruses could combine with human viruses and form a functional recombinant virus.” It’s only a matter of time. Meanwhile Abbie Smith explains why some individuals won’t develop immunity from a vaccine. She writes “Measles needs a protein on the surface of your cells in order to successfully mediate infection: CD46.” The virus must interact with this protein to infect a cell, but antibodies generated by a vaccine get in the way. Looking at the CD46 gene, researchers found that “children who had mutations at the right spot, in a particular flavor, seemed to respond better than others. But if a child had a mutation at the right spot, but not a mutation of the right flavor, they didnt respond as well.” Luckily, herd immunity can protect non-responders—as long as everyone else gets vaccinated too.
- Holy influenza, batman! on Aetiology
- ‘Not responding well to vaccines’– It is in your genes (well, partially) on ERV
Posted to the homepage on February 28, 2012.