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Repair of strand breaks by homologous recombination.

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TLDR
The enzymology of the process is discussed, followed by studies on DSB repair in living cells, and a historical context for the current view of HR is provided and how DSBs are processed during HR as well as interactions with other D SB repair pathways are described.
Abstract
In this review, we discuss the repair of DNA double-strand breaks (DSBs) using a homologous DNA sequence (i.e., homologous recombination [HR]), focusing mainly on yeast and mammals. We provide a historical context for the current view of HR and describe how DSBs are processed during HR as well as interactions with other DSB repair pathways. We discuss the enzymology of the process, followed by studies on DSB repair in living cells. Whenever possible, we cite both original articles and reviews to aid the reader for further studies.

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Journal ArticleDOI

RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1

TL;DR: It is shown that RB also localizes to DNA double-strand breaks dependent on E2F1 and ATM kinase activity and promotes DSB repair through homologous recombination (HR), and its loss results in genome instability.
Journal ArticleDOI

A role for human homologous recombination factors in suppressing microhomology-mediated end joining.

TL;DR: A role for HR genes in suppressing MMEJ in human cells is described and findings indicate that HR factors suppress mutagenic MMEj following DSB resection.
Journal ArticleDOI

Dual loss of human POLQ and LIG4 abolishes random integration

TL;DR: It is shown that DNA polymerase θ, despite its minor role in chromosomal DNA repair, substantially contributes to random integration, and that cells lacking both DNA polymerases θ and DNA ligase IV, which is essential for non-homologous end joining, exhibit 100% efficiency of spontaneous gene targeting by virtue of undetectable levels of random integration.
Journal ArticleDOI

Homology Requirements and Competition between Gene Conversion and Break-Induced Replication during Double-Strand Break Repair.

TL;DR: With short second-end homology, absence of the RecQ helicase Sgs1 promotes gene conversion, whereas deletion of the FANCM-related Mph1 helicase promotes BIR, indicating that the steps blocked by these mutations are reversible.
References
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Journal ArticleDOI

A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity.

TL;DR: This study reveals a family of endonucleases that use dual-RNAs for site-specific DNA cleavage and highlights the potential to exploit the system for RNA-programmable genome editing.
Journal ArticleDOI

Multiplex Genome Engineering Using CRISPR/Cas Systems

TL;DR: The type II prokaryotic CRISPR (clustered regularly interspaced short palindromic repeats)/Cas adaptive immune system has been shown to facilitate RNA-guided site-specific DNA cleavage as discussed by the authors.

Multiplex Genome Engineering Using CRISPR/Cas Systems

TL;DR: Two different type II CRISPR/Cas systems are engineered and it is demonstrated that Cas9 nucleases can be directed by short RNAs to induce precise cleavage at endogenous genomic loci in human and mouse cells, demonstrating easy programmability and wide applicability of the RNA-guided nuclease technology.
Journal ArticleDOI

RNA-Guided Human Genome Engineering via Cas9

TL;DR: The type II bacterial CRISPR system is engineer to function with custom guide RNA (gRNA) in human cells to establish an RNA-guided editing tool for facile, robust, and multiplexable human genome engineering.
Journal ArticleDOI

Efficient genome editing in zebrafish using a CRISPR-Cas system

TL;DR: It is shown that the CRISPR-Cas system functions in vivo to induce targeted genetic modifications in zebrafish embryos with efficiencies similar to those obtained using zinc finger nucleases and transcription activator-like effector nucleases.
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