V. Lay abstracts. Compare and suggest corrections
1) V. cholerae causes an aggressive intestine disorder in humans leading to fast dehydration and death. Drs. Silpe and Bassler developed a biological weapon against V. cholerae invasion. V. cholerae produce autoinducers that can be sensed by phages through quorum-induced receptors. Those molecules control lysis-lysogeny switch in the bacteria. The authors modeled a new protein Qtip which sequesters and inhibits phage repressor cl leading to V. cholerae cell death. This kind of technology will be able to drive lytic responses in V. cholerae with user-defined kind of signal molecules. Having such a specific kind of technology, we will be able to control certain infections and spare our microbiota.
2) As bacteria are extremely small, they have a noticeable impact on other organisms due to their quantity. Existing in large numbers, they need to coordinate group behavior. To communicate bacteria produce signal molecules, namely autoinducers, secrete them into the environment and detect signals from other bacteria. This process is called Quorum sensing (QS). QS is perhaps most well-established in Vibrio. Within the genus, Vibrio cholerae is the most dangerous as it induces the human disease cholera via QS. We recently discovered a new QS circuit in V. cholerae and other Vibrio species. The cytoplasmic receptor binds the autoinducer and therefore activates transcription of the gene encoding the small RNA (sRNA) of the gene required to form biofilms and to produce virulence factors. The ability of bacteria to infect the host organism and to produce toxins stems from their interaction with bacteriophages. Indeed, bacterial evolution largely depends on phages. This can be illustrated on the example of V. cholerae. The gene encoding the major V. cholerae virulence factor, in other words, its ability to infect the host, is located on the genome of the lysogenic temperate phage. Only V. cholerae strains containing this phage cause epidemic and pandemic cholera disease. After infecting the host cell, temperate phages can either lyse it and propagate or lysogenize it, staying inside and remaining dormant as prophages.
The ability of host signaling molecules to serve as cues to phage proteins controlling fate decisions has never been demonstrated. Here, we discover that the vibriophage is capable of responding to a host-produced autoinducer by activating the phage lytic program. To the best of our knowledge, this is the first report of a phage-encoded receptor that senses a host-produced autoinducer to mediate the lysis-lysogeny decision. Our analysis suggests that phages control their lysis-lysogeny decisions by tuning into host-produced signaling factors. We reprogramed the phage so that it responded to user-defined cues. These reprogrammable “kill switches” could be useful for environmental, industrial, and medical applications.
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