Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1992 Mar;116(5):1221-9.
doi: 10.1083/jcb.116.5.1221.

Mutants in the S. cerevisiae PKC1 gene display a cell cycle-specific osmotic stability defect

D E Levin  1 , E Bartlett-Heubusch
Affiliations

Mutants in the S. cerevisiae PKC1 gene display a cell cycle-specific osmotic stability defect

D E Levin et al. J Cell Biol. 1992 Mar.

Abstract

The PKC1 gene of Saccharomyces cerevisiae encodes a homologue of the Ca(2+)-dependent isozymes of mammalian protein kinase C (Levin, D.cE., F. O. Fields, R. Kunisawa, J. M. Bishop, and J. Thorner. 1990. Cell. 62:213-224). Cells depleted of the PKC1 gene product display a uniform phenotype, a behavior indicating a defect in the cell division cycle (cdc). These cells arrest division after DNA replication, but before mitosis. Unlike most cdc mutants, which continue to grow in the absence of cell division, PKC1-depleted cells arrest growth with small buds. We created conditional alleles of PKC1 to explore the nature of this unusual cdc defect. In contrast to PKC1-depleted cells, all of the conditional pkc1 mutants isolated were suppressed by the addition of CaCl2 to the medium, suggesting that the mutant enzymes could be activated by Ca2+. Arrest of growth and cell division in the conditional mutants was accompanied by cessation of protein synthesis, rapid loss of viability, and release of cellular material into the medium, suggesting cell lysis. This conclusion was supported by the observation that a pkc1 deletion mutant was capable of proliferation in osmotically stabilized medium, but underwent rapid cell lysis when shifted to hypo-osmotic medium. We have incorporated these observations into a model to explain the cdc-specific arrest of pkc1 mutants.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Cell. 1987 Oct 23;51(2):251-60 - PubMed
    1. J Bacteriol. 1967 May;93(5):1662-70 - PubMed
    1. J Biol Chem. 1988 May 15;263(14):6927-32 - PubMed
    1. Nature. 1987 Oct 15-21;329(6140):648-51 - PubMed
    1. Science. 1986 Jul 18;233(4761):305-12 - PubMed

Publication types

Substances