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Trends Microbiol. 2017 Jan;25(1):49-61. doi: 10.1016/j.tim.2016.09.012. Epub 2016 Oct 20.

Type III CRISPR-Cas Immunity: Major Differences Brushed Aside.

Author information

1
Institute of Biotechnology, Vilnius University, Saulėtekio av. 7, Vilnius 10257, Lithuania.
2
Institute of Biotechnology, Vilnius University, Saulėtekio av. 7, Vilnius 10257, Lithuania. Electronic address: siksnys@ibt.lt.

Abstract

For a long time the mechanism of immunity provided by the Type III CRISPR-Cas systems appeared to be inconsistent: the Type III-A Csm complex of Staphylococcus epidermidis was first reported to target DNA while Type III-B Cmr complexes were shown to target RNA. This long-standing conundrum has now been resolved by finding that the Type III CRISPR-Cas systems are both RNases and target RNA-activated DNA nucleases. The immunity is achieved by coupling binding and cleavage of RNA transcripts to the degradation of invading DNA. The base-pairing potential between the target RNA and the CRISPR RNA (crRNA) 5'-handle seems to play an important role in discriminating self and non-self nucleic acids; however, the detailed mechanism remains to be uncovered.

KEYWORDS:

CRISPR-Cas; Cmr; Csm; autoimmunity; effector complex; target RNA-activated DNA degradation

PMID:
27773522
DOI:
10.1016/j.tim.2016.09.012
[Indexed for MEDLINE]

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