RecA homologs Dmc1 and Rad51 interact to form multiple nuclear complexes prior to meiotic chromosome synapsis

Bishop, Douglas K.

doi:10.1016/0092-8674(94)90038-8

Cited by 471 publications

(527 citation statements)

References 40 publications

Supporting

Mentioning

479

Contrasting

Unclassified

Order By: Relevance

“…Cytological analysis has shown that a large fraction of Rad51 and Dmc1 foci colocalize and that normal assembly of Dmc1 foci depends on Rad51 (Bishop 1994;Dresser et al 1997;. In contrast, assembly of Rad51 foci does not appear to require Dmc1 (Bishop 1994). These cytological results suggest that both Rad51 and Dmc1 contribute to the same recombination event and that Rad51 assembles into recombination complexes whose ability to convert DSBs to recombination products depends on Dmc1.…”

Section: Rad54-mediated Repair Of Dsbs In Dmc1 Mutants Requires Disrumentioning

confidence: 95%

“…Finally, cells blocked before the DSB stage of recombination fail to form Rad51 foci at any time in meiosis (Bishop 1994;Gasior et al 1998). These four distinct phenotypes are readily observed by double staining spread nuclei with antibodies against Rad51 and tubulin.…”

Section: Analysis Of Subnuclear Rad51 Focimentioning

confidence: 98%

“…A series of observations strongly suggest that a major pathway required for conversion of meiotic DSBs to interhomologue recombination products requires the functions of both RecA homologues. Cytological analysis has shown that a large fraction of Rad51 and Dmc1 foci colocalize and that normal assembly of Dmc1 foci depends on Rad51 (Bishop 1994;Dresser et al 1997;. In contrast, assembly of Rad51 foci does not appear to require Dmc1 (Bishop 1994).…”

Section: Rad54-mediated Repair Of Dsbs In Dmc1 Mutants Requires Disrumentioning

confidence: 99%

“…Multiple subnuclear protein complexes containing Rad51 and Dmc1 can be detected as immunostaining`foci' using¯uorescence microscopy (Bishop 1994). The appearance of these foci requires DSBs because mutations in genes that block DSB formation also block formation of foci (Bishop 1994;Gasior et al 1998). In wild-type nuclei, Rad51 foci disappear in late prophase as recombination is completed.…”

Section: Introductionmentioning

confidence: 99%

“…In wild-type nuclei, Rad51 foci disappear in late prophase as recombination is completed. When repair of DSBs is blocked by a dmc1 mutation, Rad51 foci accumulate (Bishop 1994).…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

et al. 1999

Self Cite

View full text Add to dashboard Cite

Background: DMC1, the meiosis-speci®c eukaryotic homologue of bacterial recA, is required for completion of meiotic recombination and cell cycle progression past prophase. In a dmc1 mutant, double strand break recombination intermediates accumulate and cells arrest in prophase. We isolated genes which, when present at high copy numbers, suppress the meiotic arrest phenotype conferred by dmc1 mutations.

show abstract

Section: Rad54-mediated Repair Of Dsbs In Dmc1 Mutants Requires Disrumentioning

confidence: 95%

Section: Analysis Of Subnuclear Rad51 Focimentioning

confidence: 98%

Section: Rad54-mediated Repair Of Dsbs In Dmc1 Mutants Requires Disrumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In wild-type nuclei, Rad51 foci disappear in late prophase as recombination is completed. When repair of DSBs is blocked by a dmc1 mutation, Rad51 foci accumulate (Bishop 1994).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

et al. 1999

Self Cite

View full text Add to dashboard Cite

show abstract

Synaptonemal Complexes

Heyting

2002

Encyclopedia of Molecular Biology

View full text Add to dashboard Cite

Diverse roles for CDK‐associated activity during spermatogenesis

2019

View full text Add to dashboard Cite

The primary function of cyclin‐dependent kinases (CDKs) in complex with their activating cyclin partners is to promote mitotic division in somatic cells. This canonical cell cycle‐associated activity is also crucial for fertility as it allows the proliferation and differentiation of stem cells within the reproductive organs to generate meiotically competent cells. Intriguingly, several CDKs exhibit meiosis‐specific functions and are essential for the completion of the two reductional meiotic divisions required to generate haploid gametes. These meiosis‐specific functions are mediated by both known CDK/cyclin complexes and meiosis‐specific CDK‐regulators and are important for a variety of processes during meiotic prophase. The majority of meiotic defects observed upon deletion of these proteins occur during the extended prophase I of the first meiotic division. Importantly a lack of redundancy is seen within the meiotic arrest phenotypes described for many of these proteins, suggesting intricate layers of cell cycle control are required for normal meiotic progression. Using the process of male germ cell development (spermatogenesis) as a reference, this review seeks to highlight the diverse roles of selected CDKs their activators, and their regulators during gametogenesis.

show abstract

RecA homologs Dmc1 and Rad51 interact to form multiple nuclear complexes prior to meiotic chromosome synapsis

Cited by 471 publications

References 40 publications

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

Synaptonemal Complexes

Diverse roles for CDK‐associated activity during spermatogenesis

Contact Info

Product

Resources

About