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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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Genome editing with CRISPR–Cas nucleases, base editors, transposases and prime editors

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Gene therapy returns to centre stage

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CRISPR-Cas guides the future of genetic engineering.

TL;DR: The basic mechanisms that set the CRISPR-Cas toolkit apart from other programmable gene-editing technologies are described, highlighting the diverse and naturally evolved systems now functionalized as biotechnologies.
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Homologous Recombination and Human Health: The Roles of BRCA1, BRCA2, and Associated Proteins

TL;DR: This review summarizes recent findings on BRCA1, BRCa2, and associated proteins involved in human disease with an emphasis on their molecular roles and interactions.
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Recombination, Pairing, and Synapsis of Homologs during Meiosis

TL;DR: This review provides an overview of recombination-mediated processes in physical and functional linkage with meiotic axial chromosome structure, with interplay in both directions, before, during, and after formation and dissolution of the synaptonemal complex.
References
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Journal ArticleDOI

A Switch from High-Fidelity to Error-Prone DNA Double-Strand Break Repair Underlies Stress-Induced Mutation

TL;DR: This work provides evidence that the molecular basis for stress-induced mutagenesis in an E. coli model is error-prone DNA double-strand break repair (DSBR), and reveals an RpoS-controlled switch from high-fidelity to mutagenic DSBR under stress.
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An essential role for CtIP in chromosomal translocation formation through an alternative end-joining pathway

TL;DR: It is shown that depletion of CtIP, a DNA end-resection factor, results in a substantial decrease in chromosomal translocation frequency in mouse cells, and it is directly demonstrated that CtIP-mediated alt-NHEJ has a primary role in translocation formation.
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Nuclear dynamics of RAD52 group homologous recombination proteins in response to DNA damage.

TL;DR: This work shows that upon treatment of mammalian cells with ionizing radiation, RAD52 group proteins accumulate into foci at sites of DNA damage induction, and shows that these foci are dynamic structures of which Rad51 is a stably associated core component, whereas Rad52 and Rad54 rapidly and reversibly interact with the structure.
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Recognition and cleavage site of the intron-encoded omega transposase.

TL;DR: The optional group I intron of the mitochondrial 21S rRNA gene of Saccharomyces cerevisiae contains a 235-codon-long open reading frame the translation product of which (the omega transposase) catalyzes the formation of a double-strand break within the intron-minus (omega-) copies of the same gene.
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BRCA1 functions independently of homologous recombination in DNA interstrand crosslink repair.

TL;DR: It is reported that deletion of the DNA damage response factor 53BP1 overcomes embryonic lethality in Brca1-nullizygous mice and rescues HR deficiency, as measured by hypersensitivity to polyADP-ribose polymerase (PARP) inhibition.
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