Reference - PMID:9133664 - The Schizosaccharomyces pombe mra1 gene, which is required for cell growth and mating, can suppress the mating inefficiency caused by a deficit in the Ras1 activity.
Reference summary
- PubMed ID
- PMID:9133664
- Title
- The Schizosaccharomyces pombe mra1 gene, which is required for cell growth and mating, can suppress the mating inefficiency caused by a deficit in the Ras1 activity.
- Authors
- Hakuno F, Hughes DA, Yamamoto M
- Citation
- Genes Cells 1996 Mar;1(3):303-15
- Publication year
- 1996
- Abstract
- Schizosaccharomyces pombe Ras1 regulates two downstream pathways, namely the Byr2/Byr1/Spk1 mitogen-activated protein kinase cascade and the Cdc42sp small G protein pathway. The former is relevant to mating and sporulation, whereas the latter is relevant to mating, cell growth and cell morphology. We addressed whether Ras1 has any additional role in the regulation of cell physiology.
Using a specific mutation in the effector region of Ras1, we isolated a high-copy-number suppressor of the mating deficiency caused by a decrease of the Ras1 activity. The isolated gene, named mra1, encodes a novel protein of 359 amino acids, which has apparent homologues in rice and budding yeast. Disruption of mra1 indicated that it is essential for cell growth, and mutational analysis indicated that it is required for the promotion of mating. These two functions could be separated by mutations, suggesting that Mra1 is bifunctional. Overexpression of mra1 could also suppress the mating inefficiency caused by either overexpression of gap1, which is a downregulator of Ras1, or loss of function of zfs1, which is a gene relevant to the mating pheromone signalling. However, it could not suppress null mutations in genes involved in the two known pathways downstream of Ras1.
Mra1 is an apparent downstream factor of Ras1, which is essential for cell growth and relevant to mating but is not involved in the maintenance of cell morphology. Mra1 is unlikely to interact directly with the known pathways downstream of Ras1, implying that it may be a factor constituting a third pathway regulated by Ras1.
