- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Ono, B. I.
- Articles by Sando, N.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Ono, B. I.
- Articles by Sando, N.
Genetics, Vol 125, 729-738, Copyright © 1990
INVESTIGATIONS |
``Alternative Self-Diploidization'' or ``ASD'' Homothallism in Saccharomyces cerevisiae: Isolation of a Mutant, Nuclear-Cytoplasmic Interaction and Endomitotic Diploidization
B. I. Ono, Y. Ishino-Arao, K. Takasugi, M. Taniguchi, M. Fukuda, M. Fukui, I. Miyakawa and N. Sando
Laboratory of Environmental Hygiene Chemistry, Faculty of Pharmaceutical Sciences, Okayama University, Okayama 700, Japan
A mutant of Saccharomyces cerevisiae representing a novel life cycle, named ``alternative self-diploidization'' or ``ASD'' homothallism, was obtained fortuitously. In this life cycle, MAT{alpha} (or MATa) haplophase and MAT{alpha}/MAT{alpha} (or MATa/MATa) diplophase alternate. Germinated cells are haploid and mating. They soon become nonmating and sporogenous as they vegetatively grow. They sooner or later diploidize presumably via endomitosis. The diploid cells haploidize via normal meiosis. A single recessive nuclear mutation, named asd1-1, is responsible for ``ASD'' homothallism. In the {rho}(0) cytoplasm, asd1-1 cells mate even if at a low efficiency and fail to diploidize. Since pet mutations do not have such effects, we conclude that a certain mitochondrial function other than respiration is required for manifestation of ``ASD'' homothallism. That is, ``ASD'' homothallism is the result of some sort of nuclear-cytoplasmic interaction.