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The Escherichia coli RecA protein complements recombination defective phenotype of the Saccharomyces cerevisiae rad52 mutant cells.
Yeast. 2003 Apr 15; 20(5):389-96.Y

Abstract

The Saccharomyces cerevisiae rad52 mutants are sensitive to many DNA damaging agents, mainly to those that induce DNA double-strand breaks (DSBs). In the yeast, DSBs are repaired primarily by homologous recombination (HR). Since almost all HR events are significantly reduced in the rad52 mutant cells, the Rad52 protein is believed to be a key component of HR in S. cerevisiae. Similarly to the S. cerevisiae Rad52 protein, RecA is the main HR protein in Escherichia coli. To address the question of whether the E. coli RecA protein can rescue HR defective phenotype of the rad52 mutants of S. cerevisiae, the recA gene was introduced into the wild-type and rad52 mutant cells. Cell survival and DSBs induction and repair were studied in the RecA-expressing wild-type and rad52 mutant cells after exposure to ionizing radiation (IR) and methyl methanesulphonate (MMS). Here, we show that expression of the E. coli RecA protein partially complemented sensitivity and fully complemented DSB repair defect of the rad52 mutant cells after exposure to IR and MMS. We suggest that in the absence of Rad52, when all endogenous HR mechanisms are knocked out in S. cerevisiae, the heterologous E. coli RecA protein itself presumably takes over the broken DNA.

Authors+Show Affiliations

Department of Molecular Genetics, Cancer Research Institute, Slovak Academy of Sciences, Vlárska 7, 833 91 Bratislava 37, Slovak Republic.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12673622

Citation

Dudás, Andrej, et al. "The Escherichia Coli RecA Protein Complements Recombination Defective Phenotype of the Saccharomyces Cerevisiae Rad52 Mutant Cells." Yeast (Chichester, England), vol. 20, no. 5, 2003, pp. 389-96.
Dudás A, Marková E, Vlasáková D, et al. The Escherichia coli RecA protein complements recombination defective phenotype of the Saccharomyces cerevisiae rad52 mutant cells. Yeast. 2003;20(5):389-96.
Dudás, A., Marková, E., Vlasáková, D., Kolman, A., Bartosová, Z., Brozmanová, J., & Chovanec, M. (2003). The Escherichia coli RecA protein complements recombination defective phenotype of the Saccharomyces cerevisiae rad52 mutant cells. Yeast (Chichester, England), 20(5), 389-96.
Dudás A, et al. The Escherichia Coli RecA Protein Complements Recombination Defective Phenotype of the Saccharomyces Cerevisiae Rad52 Mutant Cells. Yeast. 2003 Apr 15;20(5):389-96. PubMed PMID: 12673622.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Escherichia coli RecA protein complements recombination defective phenotype of the Saccharomyces cerevisiae rad52 mutant cells. AU - Dudás,Andrej, AU - Marková,Eva, AU - Vlasáková,Danusa, AU - Kolman,Ada, AU - Bartosová,Zdena, AU - Brozmanová,Jela, AU - Chovanec,Miroslav, PY - 2003/4/4/pubmed PY - 2003/6/7/medline PY - 2003/4/4/entrez SP - 389 EP - 96 JF - Yeast (Chichester, England) JO - Yeast VL - 20 IS - 5 N2 - The Saccharomyces cerevisiae rad52 mutants are sensitive to many DNA damaging agents, mainly to those that induce DNA double-strand breaks (DSBs). In the yeast, DSBs are repaired primarily by homologous recombination (HR). Since almost all HR events are significantly reduced in the rad52 mutant cells, the Rad52 protein is believed to be a key component of HR in S. cerevisiae. Similarly to the S. cerevisiae Rad52 protein, RecA is the main HR protein in Escherichia coli. To address the question of whether the E. coli RecA protein can rescue HR defective phenotype of the rad52 mutants of S. cerevisiae, the recA gene was introduced into the wild-type and rad52 mutant cells. Cell survival and DSBs induction and repair were studied in the RecA-expressing wild-type and rad52 mutant cells after exposure to ionizing radiation (IR) and methyl methanesulphonate (MMS). Here, we show that expression of the E. coli RecA protein partially complemented sensitivity and fully complemented DSB repair defect of the rad52 mutant cells after exposure to IR and MMS. We suggest that in the absence of Rad52, when all endogenous HR mechanisms are knocked out in S. cerevisiae, the heterologous E. coli RecA protein itself presumably takes over the broken DNA. SN - 0749-503X UR - https://www.unboundmedicine.com/medline/citation/12673622/The_Escherichia_coli_RecA_protein_complements_recombination_defective_phenotype_of_the_Saccharomyces_cerevisiae_rad52_mutant_cells_ L2 - https://doi.org/10.1002/yea.971 DB - PRIME DP - Unbound Medicine ER -