Dual modes of CRISPR-associated transposon homing
Name
nihms-1716197.pdf
Description
Accepted version
Size
1.27 MB
Format
Unknown
Checksum (MD5)
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Author(s)
Saito, Makoto
Ladha, Alim
Strecker, Jonathan
Faure, Guilhem
Neumann, Edwin
Altae-Tran, Han
Macrae, Rhiannon K.
Zhang, Feng
Date Issued
March 2021
Journal
Cell
Publisher
Elsevier BV
Citation
Saito, Makoto, Ladha, Alim, Strecker, Jonathan, Faure, Guilhem, Neumann, Edwin et al. 2021. "Dual modes of CRISPR-associated transposon homing." Cell, 184 (9).
Version
Author's final manuscript
Abstract
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.
MIT Department
McGovern Institute for Brain Research at MIT
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Massachusetts Institute of Technology. Department of Biological Engineering
Howard Hughes Medical Institute
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licens
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/j.cell.2021.03.006
