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CURATOR

PhD student, Max Planck Institute for Terrestrial Microbiology

PINBOARD SUMMARY

A CRISPR-Cas complex that is able to perform all of its duties while lacking two relevant proteins.

As bacteria are constantly under attack by phages, there are several ways by which they fight back. CRISPR-Cas systems are one way, as these adaptive immune systems allow the cells to have a memory of past infections in the form of a CRISPR array, which helps to rapidly recognize and eliminate the invading threat. They do so through protein complexes that carry an specific RNA codified inside the CRISPR array (crRNA), and are able to scan through the DNA for their complementary viral target. Recognition starts by reading a 2 to 5 nucleotide sequence called Protospacer Adjacent Motif (PAM), which is located only on foreign genetic material and not in the host genome. This prevents the system from targeting itself, which would lead to cell death. To date, 6 types of CRISPR-Cas systems have been described, all with different sets of Cas proteins doing the job. We study the most widespread one, Type I, from which we specialize on a variant of the subtype Type I-F. Interestingly, this system´s complex lacks two of the Cas proteins described in other systems as essential for PAM recognition and target binding. Despite being one of the smallest complexes studied so far, it is able to fulfill the same roles as the bigger ones with comparable efficiency. Our work describes that it does so by having two newly characterized Cas proteins, that have features able to mimic the missing proteins. But why does this system exists on the first place when the other ones work so well? Viruses, in an attempt to by-pass the cell´s defenses, evolved Anti-CRISPR proteins, able to block the activity of several Type I and II complexes. For the first type, it has been described that the targets for this inhibitors are regions that are not conserved in the minimal Type I-F variant, and actually were exchanged by these two new Cas proteins. We hypothesize that the complex that we study underwent several modifications in time, in order to outsmart the counterattack by viruses, that way saving its host from death.

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