Dynamic changes in Rad51 distribution on chromatin during meiosis in male and female vertebrates

Ashley, Terry; Plug, Annemieke W.; Xu, Jihong; Solari, Alberto J.; Reddy, Gurucharan; Golub, Efim I.; Ward, David C.

doi:10.1007/bf00352222

Cited by 161 publications

(115 citation statements)

References 45 publications

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“…The two major strand exchange proteins acting in meiosis, Rad51 and Dmc1 (Shinohara 2004), have been analyzed by immunocytochemistry. In mouse and human spermatocytes and oocytes, Rad51 and Dmc1 co-localize and form multiple foci at leptotene and zygotene (Ashley et al 1995, Plug et al 1996, Barlow et al 1997, Moens et al 1997. Rad51 foci are detected in early leptotene and appear to be mostly located on the chromosome axis.…”

Section: Dsb Repair Events: An Excess Compared To Comentioning

confidence: 99%

Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis

2007

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During meiosis the programmed induction of DNA double-stranded breaks (DSB) leads to crossover (CO) and non-crossover products (NCO). One key role of CO is to connect homologs before metaphase I and thus to ensure the proper reductional segregation. This role implies an accurate regulation of CO frequency with the establishment of at least one CO per chromosome arm. Current major challenges are to understand how CO and NCO formation are regulated and what is the role of NCO. We present here the current knowledge about CO and NCO and their regulation in mammals. CO density varies widely along chromosomes and their distribution is not random as they are subject to positive interference. As documented in the mouse and human, a significant excess of DSB are generated relative to the number of CO. In fact, evidence has been obtained for the formation of NCO products, for regulation of the choice of DSB repair towards CO or NCO and for a CO specific pathway. We discuss the roles of Msh4, Msh5 and Sycp1 which affect DSB repair and probably not only the CO pathway. We suggest that, in mammals, the regulation of NCO differs from that described in Saccharomyces cerevisiae.

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Section: Dsb Repair Events: An Excess Compared To Comentioning

confidence: 99%

Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis

2007

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“…Immunostaining techniques can detect assembly of recombination proteins into subnuclear staining foci (23)(24)(25)(26)(27)(28)(29)(30)(31)(32). Several lines of evidence suggest that these foci represent protein oligomers assembled at sites of DSBs and possibly daughter strand gaps as well.…”

Section: Reca-like Recombinases Assemble On Single-strand Dna (Ssdna)mentioning

confidence: 99%

Assembly of RecA-like recombinases: Distinct roles for mediator proteins in mitosis and meiosis

Gasior

Olivares

Ear

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

158

125

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Members of the RecA family of recombinases from bacteriophage T4, Escherichia coli, yeast, and higher eukaryotes function in recombination as higher-order oligomers assembled on tracts of single-strand DNA (ssDNA). Biochemical studies have shown that assembly of recombinase involves accessory factors. These studies have identified a class of proteins, called recombination mediator proteins, that act by promoting assembly of recombinase on ssDNA tracts that are bound by ssDNA-binding protein (ssb). In the absence of mediators, ssb inhibits recombination reactions by competing with recombinase for DNA-binding sites. Here we briefly review mediated recombinase assembly and present results of new in vivo experiments. Immuno-double-staining experiments in Saccharomyces cerevisiae suggest that Rad51, the eukaryotic recombinase, can assemble at or near sites containing ssb (replication protein A, RPA) during the response to DNA damage, consistent with a need for mediator activity. Correspondingly, mediator gene mutants display defects in Rad51 assembly after DNA damage and during meiosis, although the requirements for assembly are distinct in the two cases. In meiosis, both Rad52 and Rad55͞57 are required, whereas either Rad52 or Rad55͞57 is sufficient to promote assembly of Rad51 in irradiated mitotic cells. Rad52 promotes normal amounts of Rad51 assembly in the absence of Rad55 at 30°C but not 20°C, accounting for the cold sensitivity of rad55 null mutants. Finally, we show that assembly of Rad51 is induced by radiation during S phase but not during G1, consistent with the role of Rad51 in repairing the spontaneous damage that occurs during DNA replication.H omologous recombination reactions promote repair of DNA ends formed by double-strand breaks (DSBs) and by replication fork collapse. Recombinational repair also allows cells to replicate past DNA lesions that block the progress of DNA polymerase. In phage T4, recombination is critical for initiating replication. In eukaryotes, homologous recombination is critical for accurate reductional segregation of chromosomes during meiosis. Finally, in prokaryotes, recombination allows horizontal transfer of alleles among and between bacteria and phage.At the center of homologous recombination are the recombinases, proteins that promote the formation of heteroduplex DNA. Of particular importance are the recombinases of the RecA family, including RecA in eubacteria, RadA in archea, Rad51 and Dmc1 in eukaryea, and the bacteriophage T4 UvsX protein.RecA-Like Recombinases Assemble on Single-Strand DNA (ssDNA).

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“…In addition, RAD51 homologs are expressed at relatively high levels in the reproductive organs or meiotic cells of several organisms including chicken and mouse (14,15). Furthermore, the RAD51 protein is localized to recombination foci along early meiotic chromosomes in yeast, maize, and mouse (16)(17)(18)(19) and might be a component of early recombination nodules in lily (18). Detailed analysis of RAD51 foci localization during normal and mutant maize meiosis supports the idea that RAD51 is important for homologous chromosome pairing in addition to its role in recombination (20,21).…”

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confidence: 99%

The Arabidopsis AtRAD51 gene is dispensable for vegetative development but required for meiosis

Chen

Markmann-Mulisch

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

261

328

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The maintenance of genome integrity and the generation of biological diversity are important biological processes, and both involve homologous recombination. In yeast and animals, homologous recombination requires the function of the RAD51 recombinase. In vertebrates, RAD51 seems to have acquired additional functions in the maintenance of genome integrity, and rad51 mutations cause lethality, but it is not clear how widely these functions are conserved among eukaryotes. We report here a loss-of-function mutant in the Arabidopsis homolog of RAD51, AtRAD51. The atrad51-1 mutant exhibits normal vegetative and flower development and has no detectable abnormality in mitosis. Therefore, AtRAD51 is not necessary under normal conditions for genome integrity. In contrast, atrad51-1 is completely sterile and defective in male and female meioses. During mutant prophase I, chromosomes fail to synapse and become extensively fragmented. Chromosome fragmentation is suppressed by atspo11-1, indicating that AtRAD51 functions downstream of AtSPO11-1. Therefore, AtRAD51 likely plays a crucial role in the repair of DNA doublestranded breaks generated by AtSPO11-1. These results suggest that RAD51 function is essential for chromosome pairing and synapsis at early stages in meiosis in Arabidopsis. Furthermore, major aspects of meiotic recombination seem to be conserved between yeast and plants, especially the fact that chromosome pairing and synapsis depend on the function of SPO11 and RAD51.H omologous recombination and DNA-damage repair are fundamental biological processes found in all life forms. Homologous recombination plays a major role in both maintaining genome stability (DNA-damage repair) and the generation of genetic variability. Defects in DNA-damage repair generally lead to genome instability and are increasingly found to be associated with cancer in mammals. The active surveillance mechanisms that can recognize and precisely repair DNA damage to prevent the accumulation of errors are meanwhile thought to be intimately involved in the prevention of cancer and the delaying of aging (1, 2). Genes playing critical roles in homologous recombination are important for these processes.Homologous recombination has been intensively studied in budding yeast Saccharomyces cerevisiae, and a number of genes have been identified that function in this process. Some of these genes, including RAD51, were identified based on the hypersensitivity of their mutants to radiation (3). RAD51 and another yeast gene, DMC1, share significant sequence homology with the bacterial recA gene (4). Similar to the bacterial RecA protein, the yeast RAD51 protein acts in homology searching, DNA pairing, and strand exchange (5), activities important for both DNAdamage repair and meiosis. RAD51 homologs have been found in all eukaryotic organisms thus far and are well studied in the vertebrates human, mouse, and chicken. In contrast to yeast, the loss of RAD51 function is lethal in both chicken DT40 and mouse cells (4). These RAD51-deficient cells arrest dur...

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Dynamic changes in Rad51 distribution on chromatin during meiosis in male and female vertebrates

Cited by 161 publications

References 45 publications

Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis

Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis

Assembly of RecA-like recombinases: Distinct roles for mediator proteins in mitosis and meiosis

The Arabidopsis AtRAD51 gene is dispensable for vegetative development but required for meiosis

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