The WHI1+ gene of Saccharomyces cerevisiae tethers cell division to cell size and is a cyclin homolog

Nash, R., Tokiwa, G., Anand, S., Erickson, K., Futcher, A. B. (December 1988) The WHI1+ gene of Saccharomyces cerevisiae tethers cell division to cell size and is a cyclin homolog. Embo J, 7 (13). pp. 4335-46. ISSN 0261-4189

Abstract

WHI1-1 is a dominant mutation that reduces cell volume by allowing cells to commit to division at abnormally small sizes, shortening the G1 phase of the cell cycle. The gene was cloned, and dosage studies indicated that the normal gene activated commitment to division in a dose-dependent manner, and that the mutant gene had a hyperactive but qualitatively similar function. Mild over-expression of the mutant gene eliminated G1 phase, apparently entirely relaxing the normal G1 size control, but revealing hitherto cryptic controls. Sequence analysis showed that the hyperactivity of the mutant was caused by the loss of the C-terminal third of the wild-type protein. This portion of the protein contained PEST regions, which may be signals for protein degradation. The WHI1 protein had sequence similarity to clam cyclin A, to sea urchin cyclin and to Schizosaccharomyces pombe cdc13, a cyclin homolog. Since cyclins are inducers of mitosis, WHI1 may be a direct regulator of commitment to division. A probable accessory function of the WHI1 activator is to assist recovery from alpha factor arrest; WHI1-1 mutant cells could not be permanently arrested by pheromone, consistent with a hyperactivation of division.

Item Type: Paper
Subjects: bioinformatics > genomics and proteomics > analysis and processing > Sequence Data Processing
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > cell division
organism description > yeast > Saccharomyces > Schizosaccharomyces pombe
CSHL Authors:
Communities: CSHL labs > Futcher lab
Depositing User: Gail Sherman
Date: 20 December 1988
Date Deposited: 20 Sep 2017 19:23
Last Modified: 20 Sep 2017 19:23
PMCID: PMC455150
Related URLs:
URI: https://repository.cshl.edu/id/eprint/35190

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