Understanding the Roles of Asf1 and CAF-1 in the Deactivation of the DNA Damage Checkpoint

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dc.contributor.advisor Haber, James en_US
dc.contributor.author Aguilar, Fiona
dc.date.accessioned 2014-05-12T17:45:46Z
dc.date.available 2014-05-12T17:45:46Z
dc.date.issued 2014 en_US
dc.identifier.uri http://hdl.handle.net/10192/26993
dc.description.abstract In response to a DNA double-strand break (DSB), the DNA damage checkpoint gets activated and prevents the cell from dividing while damage exists. Once repair is completed, the checkpoint gets turned off in a process termed recovery. This is important because deregulation of the checkpoint activation leads to damaged chromosomes and genomic instability, which characterize cancer predisposition. Previous research has shown that deletion of histone chaperones Asf1 and Cac1 (the largest subunit of CAF-1) reduces cell viability following induction of a DSB despite wild type levels of repair. We now focus on the effects of two DSBs vs. one DSB in the deactivation of the DNA damage checkpoint once DNA repair is completed. We show that having two DSBs exacerbates the recovery defect in asf1Δ strains, showing a phenotype similar to one observed for asf1Δcac1Δ in a one DSB background. Our data seems to suggest a correlation between the amount of DNA damage and the level of checkpoint activation. Furthermore, previous research has shown that acetylation of histone H3 on lysine 56 in S phase is a signal for recovery and is catalyzed when protein Rtt109 forms an active complex with Asf1. We conclude that deletion of Asf1 gives similar results to ones for deletion of Rtt109, so that the single deletion has some recovery phenotype, but in conjunction with CAF-1 deletion the recovery phenotype is exacerbated. en_US
dc.format.mimetype application/pdf en_US
dc.language English en_US
dc.language.iso eng en_US
dc.publisher Brandeis University en_US
dc.rights Copyright by Fiona Aguilar 2014 en_US
dc.title Understanding the Roles of Asf1 and CAF-1 in the Deactivation of the DNA Damage Checkpoint en_US
dc.type Thesis en_US
dc.contributor.department Undergraduate Program in Biology en_US
dc.degree.name BS en_US
dc.degree.level Bachelors en_US
dc.degree.discipline Biology en_US
dc.degree.grantor Brandeis University, College of Arts and Sciences en_US


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