Comparative analysis of multiple DNA double-strand break repair pathways in CRISPR-mediated endogenous tagging

Abstract CRISPR-mediated endogenous tagging is a powerful tool in biological research. Inhibiting the non-homologous end joining (NHEJ) pathway has been shown to improve the low efficiency of accurate knock-in via homology-directed repair (HDR). However, the influence of alternative double-stranded...

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Main Authors: Chiharu Tei, Shoji Hata, Akira Mabuchi, Shotaro Okuda, Kei K. Ito, Mariya Genova, Masamitsu Fukuyama, Shohei Yamamoto, Takumi Chinen, Atsushi Toyoda, Daiju Kitagawa
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-08187-5
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Summary:Abstract CRISPR-mediated endogenous tagging is a powerful tool in biological research. Inhibiting the non-homologous end joining (NHEJ) pathway has been shown to improve the low efficiency of accurate knock-in via homology-directed repair (HDR). However, the influence of alternative double-stranded break (DSB) repair pathways on knock-in remains to be fully explored. In this study, our long-read amplicon sequencing analysis reveals various patterns of imprecise repair in CRISPR-mediated knock-in, even with NHEJ inhibition. Further suppressing either microhomology-mediated end joining (MMEJ) or single-strand annealing (SSA) reduces nucleotide deletions around the cut site, thereby elevating knock-in accuracy. Additionally, imprecise donor integration is reduced by inhibiting SSA, but not MMEJ. Particularly, SSA suppression reduced asymmetric HDR, a specific imprecise integration pattern, which we further confirm using a novel reporter system. These findings demonstrate the complex interplay of multiple DSB repair pathways in CRISPR-mediated knock-in and offer novel strategies, including SSA pathway targeting, to improve precise gene editing efficiency.
ISSN:2399-3642