My thursday roundup

All is well with my tissue culture. I didn’t completely botch yesterday’s experiment (I mean all clear buffers should be ok!!!), so I’m taking some time to do read stuff that catches my eye today.

From this week’s Nature and Nature alert:

1) The platypus genome was just published. It was very interesting to see that the genome in a way reflected the major physical characteristics of the platypus. There were conserved genome regions that are similar to reptiles, birds and mammals. This isn’t something I’m normally too interested in, as I don’t have the resources to look at all this data or the knowledge to reasonably interpret it, but platypuses are just so weird, I thought it would be worth mentioning.

2) An interesting PNAS article dealing with bacterial symbionts of surgeonfish that belong to the Epulopiscium spp. The unique characteristic that really distinguishes these bacteria is their size, with individual bacterium measuring up to 600 microns (not the record holder though, that distinction goes to the “Sulfur Pearl of Namibia,” aka Thiomargarita namibiensis). This PNAS article focuses on how polyploidy, that is having multiple copies of the genome within the same organism (we’re normally diploid because we have two sets of chromosomes), correlates with the size of the bacterium.

The size of these Epulopiscium spp. is particularly interesting because bacteria are normally believed to be small due to the constraints imposed by nutrition and metabolism on organisms that don’t have specialized pathways to better exploit the environment, causing them to be smaller in order to maximize diffusion to the organism by increasing their surface to volume ratio. The authors propose that perhaps the many copies of the genome can allow compartmentalization and different functions on different regions of the cell, making it more capable of responding to complexity like eukaryotes do.

This article from Zhen et al. in Cellular Microbiology is talking about IGTP (Interferon-gamma-inducible GTPase) being able to inhibit apoptosis by signaling through FAK, which once it’s phosphorylated can bind to the SH2 domain of PI3K, then activating the PI3K/Akt pathway causing NFKB mediated expression of caspase inhibitors, etc. Interesting as I think of interferon-gamma being present in most proinflammatory contexts, so are cells actively trying not to apoptose in these environments?