The findings appeared recently in the journal Genes & Development.
Christopher Hayes, UCSB associate professor of molecular, cellular,
and development biology, teamed with graduate students Elie Diner,
Christina Beck, and Julia Webb to study uropathogenic E. coli (UPEC),
which causes urinary tract infections in humans. They discovered a
sibling-like link between cell systems that have largely been thought of
as rivals.
Associate professor Christopher Hayes and graduate student Christina Beck
The paper shows that bacteria expressing a contact--dependent growth
inhibition system (CDI) can inhibit bacteria without such a system only
if the target bacteria have CysK, a metabolic enzyme required for
synthesis of the amino acid cysteine. CysK is shown to bind to the CDI
toxin -- an enzyme that breaks RNA รณ and activate it.
For a cell system typically thought of as existing only to kill other
bacteria -- as CDIs have largely been -- the results are surprising,
said Hayes, because they suggest that a CDI+ inhibitor cell has to get
permission from its target in order to do the job.
"This is basically the inhibitor cell asking the target cell, 'Can I
please inhibit you?'" he explained. "It makes no sense. Why add an extra
layer of complexity? Why add a permissive factor? That's an unusual
finding.
"We think now that the [CDI] system is not made solely because these
cells want to go out and kill other cells," Hayes continued. "Our
results suggest the possibility that these cells may use CDI to
communicate as siblings and team up to work together; for example, in
formation of a biofilm, which lends bacteria greater strength and better
odds of survival."
The study points to the enzyme CysK as the potential catalyst to such
bacterial communication -- like a secret handshake, or a password. In
simpler terms, said Hayes, "If you have the right credentials, you're
allowed into the club; otherwise you're turned away. There's a velvet
rope, if you will, and if you're not one of the cool kids, you can't get
in."
Although only UPEC was studied for this paper, Hayes said that the
findings hold potential implications for pathogens from bacterial
meningitis to the plague, as well as for plant-based bacteria that can
devastate vegetation.
David Low, a UCSB professor of molecular, cellular, and developmental
biology and secondary author on the paper, described the work by
Hayes's laboratory as potentially groundbreaking for its insights into
how bacteria communicate -- and the practical applications that could
someday result.
"We are just starting to get some clues that bacteria may be talking
to each other with a contact-dependent language," said Low. "They touch
and respond to one another in different ways depending on the CDI
systems and other genotypic factors. Our hope is that ultimately this
work may aid the development of drugs that block or enhance
touch-dependent communication, whether the bacteria is harmful or
helpful."
The work was supported by grants from the National Institutes of Health and the National Science Foundation.
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