Compensatory role for Rad52 during recombinational repair in Ustilago maydis.

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Compensatory role for Rad52 during recombinational repair in Ustilago maydis. / Kojic, Milorad; Mao, Ninghui; Zhou, Qingwen; Lisby, Michael; Holloman, William K.

I: Molecular Microbiology, Bind 67, Nr. 5, 2008, s. 1156-68.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Kojic, M, Mao, N, Zhou, Q, Lisby, M & Holloman, WK 2008, 'Compensatory role for Rad52 during recombinational repair in Ustilago maydis.', Molecular Microbiology, bind 67, nr. 5, s. 1156-68. https://doi.org/10.1111/j.1365-2958.2008.06116.x

APA

Kojic, M., Mao, N., Zhou, Q., Lisby, M., & Holloman, W. K. (2008). Compensatory role for Rad52 during recombinational repair in Ustilago maydis. Molecular Microbiology, 67(5), 1156-68. https://doi.org/10.1111/j.1365-2958.2008.06116.x

Vancouver

Kojic M, Mao N, Zhou Q, Lisby M, Holloman WK. Compensatory role for Rad52 during recombinational repair in Ustilago maydis. Molecular Microbiology. 2008;67(5):1156-68. https://doi.org/10.1111/j.1365-2958.2008.06116.x

Author

Kojic, Milorad ; Mao, Ninghui ; Zhou, Qingwen ; Lisby, Michael ; Holloman, William K. / Compensatory role for Rad52 during recombinational repair in Ustilago maydis. I: Molecular Microbiology. 2008 ; Bind 67, Nr. 5. s. 1156-68.

Bibtex

@article{61c1b850124211ddbee902004c4f4f50,
title = "Compensatory role for Rad52 during recombinational repair in Ustilago maydis.",
abstract = "A single Rad52-related protein is evident by blast analysis of the Ustilago maydis genome database. Mutants created by disruption of the structural gene exhibited few discernible defects in resistance to UV, ionizing radiation, chemical alkylating or cross-linking agents. No deficiency was noted in spontaneous mutator activity, allelic recombination or meiosis. GFP-Rad51 foci were formed in rad52 cells following DNA damage, but were initially less intense than normal suggesting a possible role for Rad52 in formation of the Rad51 nucleoprotein filament. A search for interacting genes that confer a synthetic fitness phenotype with rad52 after DNA damage by UV irradiation identified the genes for Mph1, Ercc1 and the Rad51 paralogue Rec2. Testing known mutants in recombinational repair revealed an additional interaction with the BRCA2 orthologue Brh2. Suppression of the rec2 mutant's UV sensitivity by overexpressing Brh2 was found to be dependent on Rad52. The results suggest that Rad52 serves in an overlapping, compensatory role with both Rec2 and Brh2 to promote and maintain formation of the Rad51 nucleoprotein filament.",
author = "Milorad Kojic and Ninghui Mao and Qingwen Zhou and Michael Lisby and Holloman, {William K}",
year = "2008",
doi = "10.1111/j.1365-2958.2008.06116.x",
language = "English",
volume = "67",
pages = "1156--68",
journal = "Molecular Microbiology",
issn = "0950-382X",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - Compensatory role for Rad52 during recombinational repair in Ustilago maydis.

AU - Kojic, Milorad

AU - Mao, Ninghui

AU - Zhou, Qingwen

AU - Lisby, Michael

AU - Holloman, William K

PY - 2008

Y1 - 2008

N2 - A single Rad52-related protein is evident by blast analysis of the Ustilago maydis genome database. Mutants created by disruption of the structural gene exhibited few discernible defects in resistance to UV, ionizing radiation, chemical alkylating or cross-linking agents. No deficiency was noted in spontaneous mutator activity, allelic recombination or meiosis. GFP-Rad51 foci were formed in rad52 cells following DNA damage, but were initially less intense than normal suggesting a possible role for Rad52 in formation of the Rad51 nucleoprotein filament. A search for interacting genes that confer a synthetic fitness phenotype with rad52 after DNA damage by UV irradiation identified the genes for Mph1, Ercc1 and the Rad51 paralogue Rec2. Testing known mutants in recombinational repair revealed an additional interaction with the BRCA2 orthologue Brh2. Suppression of the rec2 mutant's UV sensitivity by overexpressing Brh2 was found to be dependent on Rad52. The results suggest that Rad52 serves in an overlapping, compensatory role with both Rec2 and Brh2 to promote and maintain formation of the Rad51 nucleoprotein filament.

AB - A single Rad52-related protein is evident by blast analysis of the Ustilago maydis genome database. Mutants created by disruption of the structural gene exhibited few discernible defects in resistance to UV, ionizing radiation, chemical alkylating or cross-linking agents. No deficiency was noted in spontaneous mutator activity, allelic recombination or meiosis. GFP-Rad51 foci were formed in rad52 cells following DNA damage, but were initially less intense than normal suggesting a possible role for Rad52 in formation of the Rad51 nucleoprotein filament. A search for interacting genes that confer a synthetic fitness phenotype with rad52 after DNA damage by UV irradiation identified the genes for Mph1, Ercc1 and the Rad51 paralogue Rec2. Testing known mutants in recombinational repair revealed an additional interaction with the BRCA2 orthologue Brh2. Suppression of the rec2 mutant's UV sensitivity by overexpressing Brh2 was found to be dependent on Rad52. The results suggest that Rad52 serves in an overlapping, compensatory role with both Rec2 and Brh2 to promote and maintain formation of the Rad51 nucleoprotein filament.

U2 - 10.1111/j.1365-2958.2008.06116.x

DO - 10.1111/j.1365-2958.2008.06116.x

M3 - Journal article

C2 - 18208529

VL - 67

SP - 1156

EP - 1168

JO - Molecular Microbiology

JF - Molecular Microbiology

SN - 0950-382X

IS - 5

ER -

ID: 3802233