Drosophila Xrcc2 regulates DNA double-strand repair in somatic cells

Bayer, Fabienne E.; Deichsel, Sebastian; Mahl, Pascal; Nagel, Anja C.

doi:10.1016/j.dnarep.2020.102807

Cited by 4 publications

(4 citation statements)

References 40 publications

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“…The protein encoded by this gene can enhance the activity of HR central protein RAD51, promote DNA damage repair, and ensure high fidelity of DNA [168]. XRCC2 is not only used as material for DNA damage repair during mitosis but also supports the DSB repair process of meiosis [169]. One study reported that XRCC2 deletion in hamster cells significantly reduced the ability for DSB-induced HR repair in vivo [170].…”

Section: Role Of Fa Genes In Poi Occurrencementioning

confidence: 99%

Research progress of the Fanconi anemia pathway and premature ovarian insufficiency

Zhao,

Zhang,

et al. 2023

Biology of Reproduction

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The Fanconi anemia pathway is a key pathway involved in the repair of deoxyribonucleic acidinterstrand crosslinking damage, which chiefly includes the following four modules: lesion recognition, Fanconi anemia core complex recruitment, FANCD2–FANCI complex monoubiquitination, and downstream events (nucleolytic incision, translesion synthesis, and homologous recombination). Mutations or deletions of multiple Fanconi anemia genes in this pathway can damage the interstrand crosslinking repair pathway and disrupt primordial germ cell development and oocyte meiosis, thereby leading to abnormal follicular development. Premature ovarian insufficiency is a gynecological clinical syndrome characterized by amenorrhea and decreased fertility due to decreased oocyte pool, accelerated follicle atresia, and loss of ovarian function in women <40 years old. Furthermore, in recent years, several studies have detected mutations in the Fanconi anemia gene in patients with premature ovarian insufficiency. In addition, some patients with Fanconi anemia exhibit symptoms of premature ovarian insufficiency and infertility. The Fanconi anemia pathway and premature ovarian insufficiency are closely associated.

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Section: Role Of Fa Genes In Poi Occurrencementioning

confidence: 99%

Research progress of the Fanconi anemia pathway and premature ovarian insufficiency

Zhao,

Zhang,

et al. 2023

Biology of Reproduction

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“…The RAD51 paralogs are conserved mediators of RAD51, supporting its function in DSB repair, meiosis, and replication (8,44). Despite their importance, the mechanistic details on how they promote HR are still unclear.…”

Section: Rad51 Paralogsmentioning

confidence: 99%

RAD51 Gene Family Structure and Function

et al. 2020

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Accurate DNA repair and replication are critical for genomic stability and cancer prevention. RAD51 and its gene family are key regulators of DNA fidelity through diverse roles in double-strand break repair, replication stress, and meiosis. RAD51 is an ATPase that forms a nucleoprotein filament on single-stranded DNA. RAD51 has the function of finding and invading homologous DNA sequences to enable accurate and timely DNA repair. Its paralogs, which arose from ancient gene duplications of RAD51, have evolved to regulate and promote RAD51 function. Underscoring its importance, misregulation of RAD51, and its paralogs, is associated with diseases such as cancer and Fanconi anemia. In this review, we focus on mammalian RAD51 structure and function and highlight the use of model systems to enable mechanistic understanding of RAD51 cellular roles. We also discuss how misregulation of the RAD51 gene family members contributes to disease and consider new approaches to pharmacologically inhibit RAD51. Expected final online publication date for the Annual Review of Genetics, Volume 54 is November 23, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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“…Effective null mutation of XRCC2 leads to a delay in (but not an absence of) RAD51 foci formation in hamster cells (Liu, 2002) and numerous studies have shown that various XRCC2 mutants are hypersensitive to DNA cross-linking agents such as mitomycin C (MMC), cisplatin, aldehydes, tirapazamine and temozolomide and that DNA replication fork dynamics are disturbed (Liu, 2002; Liu et al, 1998; Liu and Lim, 2005; Saxena et al, 2018; Wang et al, 2014). In Arabidopsis and more recently in Drosophila, XRCC2 has also been shown to be important for somatic recombination and DNA repair under genotoxic stress while having a minor or no evident role during meiosis (Bayer et al, 2020; Bleuyard et al, 2005; Da Ines et al, 2013a; Wang et al, 2014). This contrasts with mammalian studies where xrcc2 effective null mutations cause chromosome mis-segregation (Cui et al, 1999; Griffin et al, 2000; Mozdarani et al, 2001), developmental defects (Adam et al, 2007) and meiotic arrest and infertility (Griffin et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Infertility also results from a point mutation (41T>C) in human and mouse XRCC2 (Yang et al, 2018). Female Drosophila xrcc2 mutants on the other hand are fertile with normal development, which has been attributed to a postulated redundancy of the proteins XRCC2 and XRCC3 (Bayer et al, 2020). In Arabidopsis, xrcc3 null mutants are defective for meiosis, but xrcc2 null mutants are fertile and exhibit normal chromosome pairing, synapsis, and correct chromosome segregation (Bleuyard et al, 2005; Bleuyard and White, 2004; Da Ines et al, 2013a).…”

Section: Introductionmentioning

confidence: 99%

TheRAD51paralogueHvXRCC2regulates meiosis and recombination in barley

Colas,

Macaulay,

Arrieta

et al. 2023

Preprint

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Using a positional candidate-gene approach we show that semi-steriledesynaptic8mutants are associated with deletions in or complete knockout of the barley homolog ofXRCC2(X-Ray Repair Cross Complementing 2). In barleyXRCC2mutants, the initial meiotic progression is normal, albeit with a small delay in initiation, with completion of synapsis. However, the absence ofHvXRCC2subsequently leads to a dramatic reduction in the number of crossovers, chromosome mis-segregation, and infertility, suggesting thatHvXRCC2plays a major role in recombination. This mutant phenotype is congruent with that reported in mammalian studies but contrasts with theXRCC2mutant in Arabidopsis which is fertile, exhibits normal chromosome pairing and correct chromosome segregation, and is associated with an increased rate of crossovers. This indicates that theXRCC2mutant phenotype in Arabidopsis is not representative of all plants and thatXRCC2is not a good candidate for the modulation of recombination in barley.HighlightThe mutants of the barley homolog ofXRCC2exhibit delays in replication leading to defective meiosis, altered RAD51 orthologue behaviour, and significant reduction in the number of crossovers as in canonical mammalianXRCC2mutants but unlike those in Arabidopsis.

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Drosophila Xrcc2 regulates DNA double-strand repair in somatic cells

Cited by 4 publications

References 40 publications

Research progress of the Fanconi anemia pathway and premature ovarian insufficiency

Research progress of the Fanconi anemia pathway and premature ovarian insufficiency

RAD51 Gene Family Structure and Function

TheRAD51paralogueHvXRCC2regulates meiosis and recombination in barley

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