title: Type III CRISPR-Cas Immunity: Major Differences Brushed Aside.
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.
authors: Institute of Biotechnology, Vilnius University, Saulėtekio av. 7, Vilnius 10257, Lithuania.
authors: Gintautas
authors: G
authors: Tamulaitis
authors: Institute of Biotechnology, Vilnius University, Saulėtekio av. 7, Vilnius 10257, Lithuania.
authors: Česlovas
authors: Č
authors: Venclovas
authors: Institute of Biotechnology, Vilnius University, Saulėtekio av. 7, Vilnius 10257, Lithuania. Electronic address: siksnys@ibt.lt.
authors: Virginijus
authors: V
authors: Siksnys
mesh_terms: D000898:Antibiosis / Q000235:genetics*; D064113:CRISPR-Cas Systems / Q000235:genetics* / Q000502:physiology; D064112:Clustered Regularly Interspaced Short Palindromic Repeats / Q000235:genetics; D004247:DNA / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics*; D012313:RNA / Q000378:metabolism*; D016601:RNA-Binding Proteins / Q000235:genetics*; D013212:Staphylococcus epidermidis / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D016601:RNA-Binding Proteins; D012313:RNA; D004247:DNA
keywords: CRISPR-Cas; Cmr; Csm; autoimmunity; effector complex; target RNA-activated DNA degradation