Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Huang, Dongli
Mailing Address: Biology, Johns Hopkins University, 3400 N. Charles Stre, Baltimore, MD 21218, USA
Email Address: huang@jhu.edu
Phone & FAX numbers: 410-554-1224 & 410-243-6311

Abstract #15


Session Title: Chromosome Dynamics
Session Time: Wednesday, July 31 -- 9:00AM - 10:30AM
Presentation: Platform
Topic: Chromosome Dynamics

Genomic Integrity Determinants in Saccharomyces Cerevisiae .
Dongli Huang (1), Douglas Koshland (1)
(1) Department of Biology, Johns Hopkins University, Baltimore, MD 21218, Department of Embryology, Carnegie Institution of Washington, Baltimore, MD 21210

Double strand breaks (DSBs) in DNA lead to chromosome deletions and rearrangements that are a hallmark of tumor cells. Numerous studies have investigated how cells repair double strand breaks. However, little is known about the proteins that prevent double strand breaks from occurring in the first place. We call these types of proteins as genomic integrity determinants (GID). To identify GID mutants, we screened a collection of ~1900 temperature sensitive lethal mutants for those that showed an elevated loss of telomere linked markers on a 1.6Mb yeast artificial chromosome (YAC). 9 potential GID mutants were identified. We have defined a DNA elongation factor (DBP11), two DNA replication initiation proteins ORC3, ORC5 as GID proteins. In the YAC assay, the rate of terminal deletions was increased 8-24-fold by mutations in DPB11, ORC3 and ORC5. Pulsed Field Gel Electrophoresis analysis has shown that mutation in DPB11 leads to DNA breaks at a specific region, which is confirmed by chromosome I - IV translocation in dpb11cells. The removal of origins from a YAC dramatically enhanced its rate of terminal deletions in the dpb11mutant, suggesting that dpb11generates DSBs through a persistent replication fork. In contrast the removal of origins from the same YAC suppressed its rate of terminal deletions in orc3and orc5 mutants, suggesting a post-replication-initiation role of the origin recognition proteins in genomic stability.


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