Posted by It’s never made much sense to me why the pathogenic bacteria Salmonella and Shigella (which is really E. coli) have lost the ability to use lactose (milk sugar). In Shigella, we know that when we restore some lost functions through genetic manipulation (e.g., cadaverine production), they actually prevent these altered Shigella from causing disease. But lactose seems to be a good sugar to be able to grow on–they’re exposed to it from time to time (in infants).
The genus Salmonella contains two species: S. enteriditis, which causes disease* and can’t use lactose as a carbon source, and S. bongorii, which can grow on lactose and does not cause disease.
A recent study genetically engineered a S. enteritidis strain that contained the E. coli lactose utilization genes–it could grow on lactose. The authors observed that the LacI repressor, a molecule that shuts off the genes that allow growth on lactose, also inhibited the ability of S. enteritidis to cause disease, including its ability to survive in macrophages (these are immune system cells that usually gobble up and destroy bacteria and viruses, but, in the case of S. enteritidis, the bacteria usually survive in the cells and then can be released back into the body).
Interestingly, when the authors hunted through the genome of S. bongorii, they found relatives of two of the four genes involved in lactose utilization…including the LacI repressor.
Mind you, it’s not clear what exactly the LacI repressor does to prevent disease or why this would evolve (although shutting off genes activated under stressful conditions, like getting EATED!, when there’s lots of yummy sugar around strikes me as a good thing to do). Still, it will be interesting to see how many more gene losses by pathogens are, in fact, adaptations to a pathogenic life history.
*Salmonella taxonomy is a nightmare. ‘Nuff said.
June 12, 2009
June 12, 2009
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