Type III CRISPR-Cas Immunity: Major Differences Brushed Aside

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


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.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibiosis / genetics*
  • CRISPR-Cas Systems / genetics*
  • CRISPR-Cas Systems / physiology
  • Clustered Regularly Interspaced Short Palindromic Repeats / genetics
  • DNA / metabolism*
  • DNA-Binding Proteins / genetics*
  • RNA / metabolism*
  • RNA-Binding Proteins / genetics*
  • Staphylococcus epidermidis / genetics*


  • DNA-Binding Proteins
  • RNA-Binding Proteins
  • RNA
  • DNA