Type III CRISPR-Cas Immunity: Major Differences Brushed Aside

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• 作者：Gintautas Tamulaitis¹ ; Česlovas Venclovas¹ ; Virginijus Siksnys¹ ; ^{siksnys@ibt.lt}
• 关键词：CRISPR-Cas ; Csm ; Cmr ; effector complex ; target RNA-activated DNA degradation ; autoimmunity
• 刊名：Trends in Microbiology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：25
• 期：1
• 页码：49-61
• 全文大小：3244 K
• 卷排序：25

文摘

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.