E. coli K-12 is a lot like your average lab rat: predictable, well-understood, and tame. However, there’s at least one important difference between a white rat and K-12: the rat can’t mutate and become a voracious, man-eating scourge.
Okay, maybe that characterization is a little overblown. But it demonstrates the point of a new study in mBio this week: E. coli K-12 can undergo a simple mutation in an architectural protein that bestows the ability to invade human cells. From commensal to invasive in one easy step, without any major genomic flux.
Isolated almost 100 years ago from human feces, E. coli K-12 is now arguably the most completely studied microbe we know. It has lost the ability to thrive in the human gut, and when re-introduced to that environment it lives outside the human cells as a commensal, doing no harm.
Koli et al. examined a mutant E. coli K-12 they had worked with before: it has a mutation in the bacterial histone-like protein HU. Histone-like proteins modulate DNA architecture (sort of like spools do for thread, giving it some organization), so changes in these proteins can make for some pretty profound effects in how genes are regulated.
The mutation Koli et al. worked with causes a major change in how the strain transcribes certain genes, including several genes related to pathogenic interactions with mammalian cells. They introduced the mutant strain to cultures of human cells and mouse gut tissues and found it could not only get into those cells, it could replicate. The mutant also subverts the normal process of cell death in the host, allowing human cells to live longer, perhaps to allow the invading bacteria time to adapt to life inside another cell before they move on to deeper layers of tissue in the lining of the gut.
Can your Rattus norvegicus do that?