Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Genetics. 1997 Jan;145(1):63-73.

Proteolytic activation of Rim1p, a positive regulator of yeast sporulation and invasive growth.

Author information

  • 1Department of Microbiology and Institute of Cancer Research, Columbia University, New York, New York 10032, USA.

Abstract

In the yeast Saccharomyces cerevisiae, rim1, 8, 9, or 13 mutations cause four phenotypes: poor growth at low temperature, altered colony morphology, inefficient sporulation due to reduced expression of the meiotic activator IME1, and, as shown here, defective invasive growth. In this report, we have determined the relationship between RIM1 and the other genes, RIM8, 9, and 13, in this group. We have analyzed production of epitope-tagged Rim1p derivatives with HA epitopes at the N-terminus or in the middle of the protein. These Rim1p derivatives exist primarily as a small form (90 kD for Rim1-HA2p) in wild-type cells and as a large form (98 kD for Rim1-HA2p) in rim8, 9, and 13 mutants. We have also analyzed production of beta-galactosidase in strains that express a RIM1-lacZ fusion gene. beta-galactosidase exists primarily as a approximately 130 kD form in wild-type cells and as a approximately 190 kD form in rim9 mutants. These results indicate that Rim1p undergoes C-terminal proteolytic cleavage, and that rim8, 9, and 13 mutations block cleavage. Expression of a Rim1p C-terminal deletion derivative suppresses rim8, 9, and 13 mutations. Thus the phenotypes of rim8, 9, and 13 mutants arise from the defect in Rim1p C-terminal cleavage. Cleavage of Rim1p, like that of its Aspergillus nidulans homologue PacC, is stimulated under alkaline growth conditions. Therefore, Rim1p, PacC and their respective processing pathways may represent a conserved signal transduction pathway.

PMID:
9017390
[PubMed - indexed for MEDLINE]
PMCID:
PMC1207785
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk