Unstable MFs

Part of my work involves using the gpt delta transgenic mouse model, which was first described by Nohmi et al. 1996. Well Nohmi has made this into a veritable industry churning out a bunch of papers with a whole host of collaborators. There are even spin-off gpt delta transgenic rat model and the gpt delta transgenic cell line! Watch out Big Blue and MutaMouse!

Well this post has seen the light of day, perhaps not so much for its relevance to microbes (oops), but because it’s something I have to deal with. Anyway, if you are familiar with Big Blue, you’ll understand exactly how this works. Otherwise it’s convoluted and I normally have to recur to many diagrams to get it across. The gist of it is a rodent that has had bacteriophage genomes knocked in at a certain intron. The bacteriophage are not actively used by the rodent but are present in every cell of its body. It’s believed that the phage genome can be used as a reporter of the background levels of mutations perceived by the rodent.

Pseudomonas aeruginosa and microbial endocrinology

I recently presented the “Recognition of intestinal epithelial HIF-1a activation by Pseudomonas aeruginosa” by Patel et al. in a journal club discussion.  This group at the University of Chicago led by Eugene Chang and John C. Alverdy try to understand why P. aeruginosa seems to become very active in the intestines after certain surgical procedures. Their previous work described how a laparotomy (opening of the chest cavity) did not induce mortality in mice injected with PA in the cecum, while a partial hepatectomy followed by the injection caused 100% mortality. They reasoned that surgical stress made the bacteria more active (i.e. pathogenic). They focus on a gene that is important for PA’s initial opportunistic adherence called PA-I lectin/adhesin. An interesting paper in Science, which made me look into this group, shows that IFNg, an inflammatory cytokine, can bind to a surface protein of the bacterium and induce changes in transcription. They’ve also published about the effects of dynorphin, an endogeous opioid, on the bacteria’s gene expression.  In this paper, they show that hypoxia, common during surgery, sets off a chain of events that can activate PA.