The Importance of Genetic Recombination for Fidelity of Chromosome Pairing in Meiosis

Tsubouchi, Hideo; Roeder, G. Shirleen

doi:10.1016/s1534-5807(03)00357-5

Cited by 131 publications

(146 citation statements)

References 59 publications

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“…Based on earlier studies, it was suggested that the switch from intersister recombination in vegetative cells to meiotic interhomolog recombination was dependent on Dmc1 (Bishop et al 1992). However, subsequent investigations in budding yeast revealed that loss of the interhomolog recombination activity of Dmc1 could be overcome by overexpression of Rad51 or Rad54, which stimulates Rad51 activity, indicating that, in this species at least, the specificity of repair partner choice during meiosis does not entirely rest on Dmc1 (Bishop et al 1999;Tsubouchi and Roeder 2003). This is supported by work that has revealed several proteins that are important regulators of this process in budding yeast.…”

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confidence: 99%

ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis

Sanchez‐Moran¹,

Santos²,

Jones³

et al. 2007

Genes Dev.

245

326

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ASY1 is an Arabidopsis protein required for synapsis and crossover formation during meiosis. The chronology of meiotic recombination has been investigated in wild type and an asy1 mutant. We observe a delay between the appearance of chromatin-associated AtSPO11-1 foci and DNA double-strand break (DSB) formation, which occurs contemporaneously with chromosome axis formation and transition of ASY1 from chromatin-associated foci to a linear axis-associated signal. DSBs are formed independently of ASY1 in an AtSPO11-1-dependent manner. They are partially restored in Atspo11-1-3 using cisplatin, but their control appears abnormal. Axis morphogenesis is independent of ASY1, but axis structure may be compromised in asy1. Localization of the strand exchange proteins AtRAD51 and AtDMC1 to the chromatin occurs asynchronously shortly after DSB formation, with AtDMC1 localizing in advance of AtRAD51. In wild-type nuclei, both recombinases form numerous foci that persist for ∼12 h before gradually decreasing in number. In asy1, initial localization of AtDMC1 is normal, but declines abruptly such that interhomolog recombination is severely compromised. Limited ASY1-independent, DMC1-dependent interhomolog recombination remains, but appears restricted to subtelomeric sequences where the homologs are fortuitously in proximity. Thus, ASY1 plays a key role in coordinating the activity of the RecA homologs to create a bias in favor of interhomolog recombination.

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confidence: 99%

ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis

Sanchez‐Moran¹,

Santos²,

Jones³

et al. 2007

Genes Dev.

245

326

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“…In Saccharomyces cerevisiae there appear to be two distinct meiotic recombination pathways, with one being dependent on Rad51 alone (referred to as the Rad51-only pathway) and the other on both Rad51 and Dmc1 (called the Dmc1-dependent pathway) (Tsubouchi and Roeder 2003). While Rad51 alone is able to repair meiotic DSBs, it has been demonstrated that coordinated function of Rad51 and Dmc1 is required to achieve the meiosis-specific bias for interhomolog recombination (Sheridan and Bishop 2006).…”

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Hed1 regulates Rad51-mediated recombination via a novel mechanism

Busygina¹,

Sehorn²,

Shi³

et al. 2008

Genes Dev.

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104

139

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Two RecA orthologs, Rad51 and Dmc1, mediate homologous recombination in meiotic cells. During budding yeast meiosis, Hed1 coordinates the actions of Rad51 and Dmc1 by down-regulating Rad51 activity. It is thought that Hed1-dependent attenuation of Rad51 facilitates formation of crossovers that are necessary for the correct segregation of chromosomes at the first meiotic division. We purified Hed1 in order to elucidate its mechanism of action. Hed1 binds Rad51 with high affinity and specificity. We show that Hed1 does not adversely affect assembly of the Rad51 presynaptic filament, but it specifically prohibits interaction of Rad51 with Rad54, a Swi2/Snf2-like factor that is indispensable for Rad51-mediated recombination. In congruence with the biochemical results, Hed1 prevents the recruitment of Rad54 to a site-specific DNA double-strand break in vivo but has no effect on the recruitment of Rad51. These findings shed light on the function of Hed1 and, importantly, unveil a novel mechanism for the regulation of homologous recombination.[Keywords: Regulation of meiotic recombination; interhomolog crossovers; Rad51 recombinase; double-strand break repair; homologous recombination] Supplemental material is available at http://www.genesdev.org.

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“…The hop2 deletion mutant in S. cerevisiae fails to sporulate due to a uniform arrest at the pachytene stage of meiosis I with most of the chromosomes engaged in synapsis with nonhomologous partners (22). This meiotic cell cycle arrest by the hop2 mutation is bypassed by the dmc1 mutation, indicating that the meiotic arrest of hop2 is due to the action of the Dmc1 protein (25). This genetic interaction between HOP2 and DMC1 suggests that the Hop2 protein functions in the strand invasion step, which is promoted by the Dmc1 protein, during meiosis.…”

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confidence: 99%

Positive Role of the Mammalian TBPIP/HOP2 Protein in DMC1-mediated Homologous Pairing

Enomoto¹,

Kinebuchi²,

Sato

et al. 2004

Journal of Biological Chemistry

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In meiosis, homologous recombination preferentially occurs between homologous chromosomes rather than between sister chromatids, which is opposite to the bias of mitotic recombinational repair. The TBPIP/HOP2 protein is a factor that ensures the proper pairing of homologous chromosomes during meiosis. In the present study, we found that the purified mouse TBPIP/ HOP2 protein stimulated homologous pairing catalyzed by the meiotic DMC1 recombinase in vitro. In contrast, TBPIP/HOP2 did not stimulate homologous pairing by RAD51, which is another homologous pairing protein acting in both meiotic and mitotic recombination. The positive effect of TBPIP/HOP2 in the DMC1-mediated homologous pairing was only observed when TBPIP/ HOP2 first binds to double-stranded DNA, not to singlestranded DNA, before the initiation of the homologous pairing reaction. Deletion analyses revealed that the C-terminal basic region of TBPIP/HOP2 is required for efficient DNA binding and is also essential for its homologous pairing stimulation activity. Therefore, these results suggest that TBPIP/HOP2 directly binds to DNA and functions as an activator for DMC1 during the homologous pairing step in meiosis.During meiosis, two successive rounds of nuclear division, meiosis I and meiosis II, are promoted with a single round of DNA replication. As a result, diploid cells produce haploid gametes in eukaryotes. In the cell division at meiosis I, homologous chromosomes are aligned, and a high level of recombination occurs between homologous chromosomes but not between sister chromatids. This preferential recombination between homologous chromosomes, called homologous recombination, ensures their correct segregation at meiosis I through the formation of chiasmata, which physically connect homologous chromosomes.Homologous recombination is initiated by double strand break (DSB) 1 formation by SPO11 at the initiation sites for recombination (1-3). Then a single-stranded DNA (ssDNA) tail derived from a DSB site invades the homologous doublestranded DNA (dsDNA) to form a heteroduplex. This strand invasion step, called homologous pairing, is the key step in homologous recombination. In Escherichia coli, the RecA protein catalyzes the homologous pairing step (4, 5). Two eukaryotic homologues of RecA, the RAD51 and DMC1 proteins, which are conserved from yeast to human, have been identified (6 -9) and have been shown to catalyze homologous pairing in vitro (10 -15). The RAD51 gene is expressed in both mitotic and meiotic cells, but the DMC1 gene functions only in meiotic cells. Disruption of the Rad51 gene results in early embryonic lethality in mice (16,17). In chicken DT40 cells, the RAD51 gene disruption causes the accumulation of spontaneous chromosomal breaks and significantly reduces the recombination frequency between sister chromatids (18,19). In contrast, disruption of the Dmc1 gene does not cause lethality in mice, but the dmc1 knock-out mice are sterile with an arrest of gametogenesis in the first meiotic prophase (20,21). Therefore, DMC1 is a me...

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The Importance of Genetic Recombination for Fidelity of Chromosome Pairing in Meiosis

Cited by 131 publications

References 59 publications

ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis

ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis

Hed1 regulates Rad51-mediated recombination via a novel mechanism

Positive Role of the Mammalian TBPIP/HOP2 Protein in DMC1-mediated Homologous Pairing

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