« Previous AbstractOlfactory response of Trichogramma pretiosum (Hymenoptera: Trichogrammatidae) to volatiles induced by transgenic maize    Next AbstractVolatile molecules from bronchoalveolar lavage fluid can 'rule-in' Pseudomonas aeruginosa and 'rule-out' Staphylococcus aureus infections in cystic fibrosis patients »

EMBO J

Title:		The WHI1+ gene of Saccharomyces cerevisiae tethers cell division to cell size and is a cyclin homolog
Author(s):		Nash R; Tokiwa G; Anand S; Erickson K; Futcher AB;
Address:		"Cold Spring Harbor Laboratory, NY 11724"
Journal Title:		EMBO J
Year:		1988
Volume:		7
Issue:		13
Page Number:		4335 - 4346
DOI:		10.1002/j.1460-2075.1988.tb03332.x
ISSN/ISBN:		0261-4189 (Print) 1460-2075 (Electronic) 0261-4189 (Linking)
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"
Keywords:		"Amino Acid Sequence Base Sequence Cell Cycle/drug effects Cell Division Cloning, Molecular DNA, Fungal/genetics Genes, Dominant *Genes, Fungal Mating Factor Molecular Sequence Data Mutation Nuclear Proteins/genetics Peptides/pharmacology Phenotype Prolife;"
Notes:		"MedlineNash, R Tokiwa, G Anand, S Erickson, K Futcher, A B eng GM39978/GM/NIGMS NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. England 1988/12/20 EMBO J. 1988 Dec 20; 7(13):4335-46. doi: 10.1002/j.1460-2075.1988.tb03332.x"