sitting on these for a while

The ecology and biotechnology of sulphate-reducing bacteria

Nature reviews microbiology 2008

Muyzer and Stams

Sulphate-reducing bacteria can use sulphate as a terminal electron acceptor (sulphate acts as an oxidant and gets reduced). SRBs are anoxic and impact the sulphur cycle which can impact the carbon cycle. It’s important in the corrosion of heavy metals in pipes but also it could be used in biotechnology. another interesting facet of their biotechnology is that they have to be cocultured at times to create slightly anoxic microenvironments in which they can thrive, so they’re interesting from the perspective of the metabolic web they establish.

Host cell processes that influence the intracellular survival of Legionella pneumophila

Cellular Microbiology 2008

Shin and Roy

L. pneumophila has processes that allow it to survive and replicate within protozoa, which also allow it to do so in macrophages within specific vacuoles. It uses a type four secretion system to move bacterial effectors into the cell. The effects of this are changes in host cell processes, such as the altering the trafficking of the phagosome and mediating its conversion into an ER-derived organelle permissive for the bacteria. The effector proteins in the highly plastic genome contain many eukaryotic protein motifs, which are well conserved among eukaryotes, which explains the ease by which LP can affect humans. DOT/ICM genes are the famous ones in this. Host factors are recruited to the LCV and disrupt vesicle traffic. LP can also affect apoptosis pathways to its benefit, in order to allow for more replication. Eukaryotes have developed skills that allow them to fight back

Bacterial-modulated signaling pathways in gut homeostasis

Perspective in STKE

Lee 2008

Commensal bugs in the gut are known to affect innate immunity and development. In order to avoid excess inflammation, some bugs have developed ways to modulate host intracellular signaling pathways. Bacteria induced ROS which inhibit cullin-1dependent protein degradation which stabilizes IKB, a negative regulator of inflammation. NFKB modulation seems to be a big strategy by which commensals reduce gut inflammation. Bacteria have also developed ways to stabilize another regulator B catenin (stopping the degradation machinery prevents B catenin ubiquitination). Interesting to start thinking about these interactions we have with ~500 prokaryotic species comprising 10^14 bugs.

Jeffrey Gordon

I heard a talk by Dr. Jeffrey Gordon, not Jeff Gordon, for those of you wondering. I was pretty excited about the talk because Dr. Gordon has been putting out some very interesting work concerning the human microbiome and the role of microbial communities in our gut in determining how the host responds to its environmental conditions and diseases.

The talk was very well attended, a testament to the interest in this new field. Dr. Gordon, as seems to be the custom nowadays, introduced the concept that we are more bacterial than eukaryotic, at least by sheer number of cells. I think he mentioned we are 90% microbial and 10% “us” and referred to the collective organism as a supra-organism.

The largest diversity of microorganisms living in our body are located in our gastrointestinal tract. Dr. Gordon alluded to the fact that the modern world with the ability to travel from one place to another, the exposure to many different kinds of foods and the 60 years in which humans have been regularly using antibiotics can really affect the diversity of bacteria in our gut.

2 out of the 100 phyla of bacteria known dominate. These are the firmicutes and the bacteroidetes. There are 8 others in smaller proportion. There is at least one Archaeon. There might be more phages than bacteria in our gut!

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.

Timers and blots

All day today I was held captive by the whims of my taskmaster, the timer.

I am so utterly tired.  Every 15-20 minutes… beep, beep, beep.  Growing bacteria, incubating this or that, shaking bugs, checking the autoclave, washing blots, etc.  Tuesdays on a gpt week are tough.  I was so tired I couldn’t even think of multitasking!  The very thought was incapacitating, and I had to do things one step at a time!

Anyway, on better news, I think my Southern blots finally worked.  ECL kits are so much easier to use than the Pierce North2South!

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.