ArticleGenetics2004
A novel gene, msa1, inhibits sexual differentiation in Schizosaccharomyces pombe.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The Fission Yeast Cell Integrity Pathway: A Functional Hub for Cell Survival upon Stress and Beyond.Journal of fungi (Basel, Switzerland) · 2021Review
- Phosphorylation of the RNA-binding protein Zfs1 modulates sexual differentiation in fission yeast.Journal of cell science · 2017Article
- TORC1 and TORC2 converge to regulate the SAGA co-activator in response to nutrient availability.EMBO reports · 2017Article
- The RNA binding protein Csx1 promotes sexual differentiation in Schizosaccharomyces pombe.PloS one · 2012Article
- Role of the RNA-binding protein Nrd1 in stress granule formation and its implication in the stress response in fission yeast.PloS one · 2012Article
- Multistep regulation of protein kinase A in its localization, phosphorylation and binding with a regulatory subunit in fission yeast.Current genetics · 2011Article
- Regulation and role of an RNA-binding protein Msa2 in controlling the sexual differentiation of fission yeast.Current genetics · 2011Article
- Article
- Article
- Moc3, a novel Zn finger type protein involved in sexual development, ascus formation, and stress response of Schizosaccharomyces pombe.Current genetics · 2005Article
- Role for RNA-binding proteins implicated in pathogenic development of Ustilago maydis.Eukaryotic cell · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sexual differentiation in the fission yeast Schizosaccharomyces pombe is triggered by nutrient starvation or by the presence of mating pheromones. We identified a novel gene, msa1, which encodes a 533-aa putative RNA-binding protein that inhibits sexual differentiation. Disruption of the msa1 gene caused cells to hypersporulate. Intracellular levels of msa1 RNA and Msa1 protein diminished after several hours of nitrogen starvation. Genetic analysis suggested that the function of msa1 is independent of the cAMP pathway and stress-responsive pathway. Deletion of the ras1 gene in diploid cells inhibited sporulation and in haploid cells decreased expression of mating-pheromone-induced genes such as mei2, mam2, ste11, and rep1; simultaneous deletion of msa1 reversed both phenotypes. Overexpression of msa1 decreased activated Ras1(Val17)-induced expression of mam2. Phenotypic hypersporulation was similar between cells with deletion of only rad24 and both msa1 and rad24, but simultaneous deletion of msa1 and msa2/nrd1 additively increased hypersporulation. Therefore, we suggest that the primary function of Msa1 is to negatively regulate sexual differentiation by controlling the expression of Ste11-regulated genes, possibly through the pheromone-signaling pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.