How E. coli chats

Friday, 23 June, 2017

They can’t use smartphones or Wi-Fi, but bacteria have evolved some seriously complex strategies to communicate with one another. And the resulting interactions are a delicate balance of cooperation and, in some cases, competition. Biologists have uncovered a new way that bacteria lay siege to neighbouring cells by hijacking two factors involved in protein synthesis.

These intraspecies exchanges take place within contact-dependent growth inhibition systems, which regulate cellular activities via cell-to-cell contact and are found in a wide variety of gram-negative bacteria, including important human pathogens such as Escherichia coli.

UC Santa Barbara biologists examined how E. coli EC869, which causes diarrhoea or haemorrhagic colitis in humans, destroys its neighbours by transferring toxins that inhibit their cell growth. Previous work by other UCSB researchers had shown that a different variation of E. coli required a ‘permissive factor’ for toxin activation. Did EC869 also needed to bind protein in the target cell to activate its toxin the researchers wondered.

The answer is yes, with a twist.

Many toxins inhibit translation, the essential process by which the sequence of messenger RNA (mRNA) is converted into protein. Some toxins accomplish this by breaking transfer RNAs (tRNAs), molecules that help decode mRNA sequences.

The UCSB team discovered that the EC869 toxin binds to the most abundant protein in bacteria, elongation factor Tu (EF-Tu). EF-Tu’s role in protein synthesis is to bind to tRNA molecules. The binding action not only activates toxins but also helps zero in on the true target: tRNA molecules. And not just any tRNA: EC869 cleaves only two specific tRNA molecules out of 46 types present in the cell.

This class of toxins only cuts specific tRNA molecules and the researchers hypothesise that the toxins sit bound to EF-Tu as different tRNA molecules are loaded and unloaded until the specific target arrives. Once the right tRNA is loaded, it is cleaved, destabilised and released.

It will be interesting to see if the interaction of this toxin with members of the protein synthesis apparatus plays a role in intercellular communication.

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