反式激活crRNA
清脆的
生物
转座因子
转座酶
计算生物学
核糖核酸
睡美人转座系统
换位(逻辑)
归巢(生物学)
Cas9
CRISPR干扰
遗传学
基因
细胞生物学
基因组
基因驱动
质粒
流动遗传元素
DNA
计算机科学
语言学
哲学
人工智能
生态学
作者
Makoto Saito,Alim Ladha,Jonathan Strecker,Guilhem Faure,Edwin N. Neumann,Han Altae-Tran,Rhiannon K. Macrae,Feng Zhang
出处
期刊:Cell
[Elsevier]
日期:2021-04-01
卷期号:184 (9): 2441-2453.e18
被引量:72
标识
DOI:10.1016/j.cell.2021.03.006
摘要
Tn7-like transposons have co-opted CRISPR systems, including class 1 type I-F, I-B, and class 2 type V-K. Intriguingly, although these CRISPR-associated transposases (CASTs) undergo robust CRISPR RNA (crRNA)-guided transposition, they are almost never found in sites targeted by the crRNAs encoded by the cognate CRISPR array. To understand this paradox, we investigated CAST V-K and I-B systems and found two distinct modes of transposition: (1) crRNA-guided transposition and (2) CRISPR array-independent homing. We show distinct CAST systems utilize different molecular mechanisms to target their homing site. Type V-K CAST systems use a short, delocalized crRNA for RNA-guided homing, whereas type I-B CAST systems, which contain two distinct target selector proteins, use TniQ for RNA-guided DNA transposition and TnsD for homing to an attachment site. These observations illuminate a key step in the life cycle of CAST systems and highlight the diversity of molecular mechanisms mediating transposon homing.
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