Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663630
Title: Genetic and molecular analysis of the wis2+ gene in fission yeast
Author: Weisman, Ronit
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1994
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Abstract:
The wis1+-wis5+ genes of the fission yeast Schizosaccharomyces pombe were isolated as multicopy suppressers of the cell cycle defect of the triple mutant wee1-50 cdc25-22 win1-1. The wee-1 and cdc25cdc25+ gene products are negative and positive regulators, respectively, of p34cdc2 protein kinase, the key regulator of entry into mitosis. The interaction of win1-1 with mitotic control genes suggests that win1+ plays a role in the control over entry into mitosis. The work described in this thesis is primarily concerned with the genetic and molecular analysis of the wis2+ gene. DNA sequence analysis of wis2+ showed that it encodes a novel cyclophilin-like protein with the predicted molecular weight of 40 kDa. The predicted protein represents an unusual cyclophilin as the 18 kDa cyclophilin domain is followed by a C-terminal domain of 188 amino acid. Cyclophilins have been implicated in two separate cellular processes. One is protein folding and transport; the other is the blockage of signal transduction pathways when complexed with the immunosuppressive drug cyclosporin A. The only genetic interaction detected that involves the wis2+ gene is the suppression of the cell cycle defect of wee1-50 cdc25-22 win1-1 by overexpression (referred to as wis2 activity). No effect associated with either overexpression or deletion of wis2+ has been observed in either wild type strains or in a variety of cell cycle mutant strains. Structure-function analysis has been carried out in order to determine the role of the two distinct regions of wis2+ in wis2 activity.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.663630  DOI: Not available
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