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Hi all!

I have chosen this paper, because I think it is an interesting topic and also because we have not had anything on Streptomyces yet. Furthermore since this work, is from a former student of my supervisor, and she is willing to attend the session and so will Paul. So we get some input from the researcher directly! 

Hopefully see many of you on the 2nd of April at 8 pm BST! 

Here it goes:

Mammalian cell entry genes in Streptomyces may provide clues to the evolution of bacterial virulence

This week’s Journal Club is on a publication on how virulence might have evolved in bacteria. The non-pathogenic soil bacterium S. coelicolor, nevertheless in their genome you can find homologues of virulence loci. This paper investigates the mammalian cell entry locus (mce) in S. coelicolor, it has previously been characterised in M. tuberculosis. The study investigates its impact on cell survival, morphology and interaction with other soil organisms (A. polyphaga and Arabidopsis). The results suggest that the genes play an important role in survival in the environment and give hints into the evolution and selection as these genes as virulence factors.

Discussion points:

–          Was the publication easy to read/follow/understand?

–          Do you think this research is helping to understand how virulence evolved?

–          Which follow up experiments could be done based on the data presented?


The paper up for discussion on Tuesday 19th March, 8pm UK time is on Helicobacter and can be found here

Author summary:

Helicobacter pylori is a bacterium that colonizes the stomach of about half the world’s population, most of whom are asymptomatic. However, some strains of H. pylori express a bacterial secretion system, a sort of molecular syringe that injects a bacterial protein inside the gastric cells and causes inflammation that can lead to peptic ulcer disease or gastric cancer. One of the essential components of the H. pylori secretion system is CagY, which is unusual because it contains a series of repetitive amino acid motifs that are encoded by a very large number of direct DNA repeats. Here we have shown that DNA recombination in cagY changes the protein motif structure and alters the function of the secretion system turning it on or off. Using mouse and non-human primate models, we have demonstrated that CagY is a molecular switch that ‘‘tunes’’ the host inflammatory response, and likely contributes to persistent infection. Determining the mechanism by which CagY functions will enhance our understanding of the effects of H. pylori on human health, and could lead to novel applications for the modulation of host cell function.

Discussion points:

1. Is the paper well written, easy to understand and follow?

2. CagY variants evade the hosts immune response, any thoughts?

3. Is inflammation advantageous?

4. Anything you would do differently?