Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

RELATIONSHIPS BETWEEN A HYPER-REC MUTATION (rem1) AND OTHER RECOMBINATION AND REPAIR GENES IN YEAST

RELATIONSHIPS BETWEEN A HYPER-REC MUTATION (rem1) AND OTHER RECOMBINATION AND REPAIR GENES IN YEAST ABSTRACT Mutations in the REM1 gene of Saccharomyces cerevisiae confer a semidominant hyper-recombination and hypermutable phenotype upon mitotic cells (Golin and Esposito 1977). These effects have not been observed in meiosis. We have examined the interactions of rem1 mutations with rad6-1, rad50-1, rad52-1 or spo11-1 mutations in order to understand the basis of the rem1 hyper-rec phenotype. The rad mutations have pleiotropic phenotypes; spo11 is only defective in sporulation and meiosis. The RAD6, RAD50 and SPO11 genes are not required for spontaneous mitotic recombination; mutations in the RAD52 gene cause a general spontaneous mitotic Rec- phenotype. Mutations in RAD50, RAD52 or SPO11 eliminate meiotic recombination, and mutations in RAD6 prevent spore formation. Evidence for the involvement of RAD6 in meiotic recombination is less clear. Mutations in all three RAD genes confer sensitivity to X rays; the RAD6 gene is also required for UV damage repair. To test whether any of these functions might be involved in the hyper-rec phenotype conferred by rem1 mutations, double mutants were constructed. Double mutants of rem1 spo11 were viable and demonstrated rem1 levels of mitotic recombination, suggesting that the normal meiotic recombination system is not involved in producing the rem1 phenotype. The rem1 rad6 double mutant was also viable and had rem1 levels of mitotic recombination. Neither rem1 rad50 nor rem1 rad52 double mutants were viable. This suggests that rem1 causes its hyper-rec phenotype because it creates lesions in the DNA that are repaired using a recombination-repair system involving RAD50 and RAD52. This content is only available as a PDF. © Genetics 1984 This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genetics Oxford University Press

RELATIONSHIPS BETWEEN A HYPER-REC MUTATION (rem1) AND OTHER RECOMBINATION AND REPAIR GENES IN YEAST

Malone, Robert E; Hoekstra, Merl F
Genetics , Volume 107 (1) – May 1, 1984
Download PDF
16 pages

Loading next page...
 
/lp/oxford-university-press/relationships-between-a-hyper-rec-mutation-rem1-and-other-Qbth53FEyb

References (26)

Publisher
Oxford University Press
Copyright
Copyright © 2021 Genetics Society of America
ISSN
0016-6731
eISSN
1943-2631
DOI
10.1093/genetics/107.1.33
Publisher site
See Article on Publisher Site

Abstract

ABSTRACT Mutations in the REM1 gene of Saccharomyces cerevisiae confer a semidominant hyper-recombination and hypermutable phenotype upon mitotic cells (Golin and Esposito 1977). These effects have not been observed in meiosis. We have examined the interactions of rem1 mutations with rad6-1, rad50-1, rad52-1 or spo11-1 mutations in order to understand the basis of the rem1 hyper-rec phenotype. The rad mutations have pleiotropic phenotypes; spo11 is only defective in sporulation and meiosis. The RAD6, RAD50 and SPO11 genes are not required for spontaneous mitotic recombination; mutations in the RAD52 gene cause a general spontaneous mitotic Rec- phenotype. Mutations in RAD50, RAD52 or SPO11 eliminate meiotic recombination, and mutations in RAD6 prevent spore formation. Evidence for the involvement of RAD6 in meiotic recombination is less clear. Mutations in all three RAD genes confer sensitivity to X rays; the RAD6 gene is also required for UV damage repair. To test whether any of these functions might be involved in the hyper-rec phenotype conferred by rem1 mutations, double mutants were constructed. Double mutants of rem1 spo11 were viable and demonstrated rem1 levels of mitotic recombination, suggesting that the normal meiotic recombination system is not involved in producing the rem1 phenotype. The rem1 rad6 double mutant was also viable and had rem1 levels of mitotic recombination. Neither rem1 rad50 nor rem1 rad52 double mutants were viable. This suggests that rem1 causes its hyper-rec phenotype because it creates lesions in the DNA that are repaired using a recombination-repair system involving RAD50 and RAD52. This content is only available as a PDF. © Genetics 1984 This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Journal

Genetics – Oxford University Press

Published: May 1, 1984

There are no references for this article.