Modeling Cell Cycle Effects of Human 14-3-3 Tumor Promoting Proteins in Saccharomyces Cerevisiae

Persistent Link:
http://hdl.handle.net/10150/244407
Title:
Modeling Cell Cycle Effects of Human 14-3-3 Tumor Promoting Proteins in Saccharomyces Cerevisiae
Author:
Liu, Natalie; Putnam, Charles W.; Martinez, Jesse D.
Issue Date:
May-2012
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
In this study, we used budding yeast as a model organism to examine the effects of overexpression of Bmh1, a yeast homolog of 14-3-3γ. We found that in the presence of modest DNA damage, Bmh1 overexpression had its most prominent effect during G2/M-phase of the cell cycle. We also observed that overexpression of Bmh1 concurrent with the induction of DNA damage partially rescued the G2/M arrest defect caused by the absence of Rad9, a key component of the G2/M DNA damage checkpoint pathway. When RAD53, a gene in the "Rad53 pathway" of the G2/M checkpoint, was deleted, overexpression of Bmh1 had no effect. However, overexpression of Bmh1 in a strain bearing the rad53-11 mutation partially rescued the arrest. Additionally, Bmh1 overexpression had a minimal effect on the G2/M arrest response with deletion of Chk1, a key component of the parallel G2/M checkpoint pathway. This led us to hypothesize that overexpression of Bmh1in the absence of Rad9 modulates the Rad53 pathway. We propose a model in which the rescue of Rad9’s otherwise obligatory role in the DNA damage checkpoint is the consequence of Bmh1 subserving the adaptor function of Rad9 by bringing Mec1 and Rad53 together.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
bachelors
Degree Program:
Honors College; Molecular and Cellular Biology
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleModeling Cell Cycle Effects of Human 14-3-3 Tumor Promoting Proteins in Saccharomyces Cerevisiaeen_US
dc.creatorLiu, Natalieen_US
dc.contributor.authorLiu, Natalieen_US
dc.contributor.authorPutnam, Charles W.en_US
dc.contributor.authorMartinez, Jesse D.en_US
dc.date.issued2012-05-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractIn this study, we used budding yeast as a model organism to examine the effects of overexpression of Bmh1, a yeast homolog of 14-3-3γ. We found that in the presence of modest DNA damage, Bmh1 overexpression had its most prominent effect during G2/M-phase of the cell cycle. We also observed that overexpression of Bmh1 concurrent with the induction of DNA damage partially rescued the G2/M arrest defect caused by the absence of Rad9, a key component of the G2/M DNA damage checkpoint pathway. When RAD53, a gene in the "Rad53 pathway" of the G2/M checkpoint, was deleted, overexpression of Bmh1 had no effect. However, overexpression of Bmh1 in a strain bearing the rad53-11 mutation partially rescued the arrest. Additionally, Bmh1 overexpression had a minimal effect on the G2/M arrest response with deletion of Chk1, a key component of the parallel G2/M checkpoint pathway. This led us to hypothesize that overexpression of Bmh1in the absence of Rad9 modulates the Rad53 pathway. We propose a model in which the rescue of Rad9’s otherwise obligatory role in the DNA damage checkpoint is the consequence of Bmh1 subserving the adaptor function of Rad9 by bringing Mec1 and Rad53 together.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplineMolecular and Cellular Biologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
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