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The G1 DNA damage checkpoint in Sacc...

Fitz Gerald, Jonathan Nesbit.

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The G1 DNA damage checkpoint in Saccharomyces cerevisiae.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The G1 DNA damage checkpoint in Saccharomyces cerevisiae./
作者:	Fitz Gerald, Jonathan Nesbit.
面頁冊數:	160 p.
附註:	Adviser: Stephen J. Kron.
Contained By:	Dissertation Abstracts International63-01B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3039067
ISBN:	0493525300

The G1 DNA damage checkpoint in Saccharomyces cerevisiae.
Fitz Gerald, Jonathan Nesbit.

The G1 DNA damage checkpoint in Saccharomyces cerevisiae. - 160 p.

Adviser: Stephen J. Kron.

Thesis (Ph.D.)--The University of Chicago, 2002.

Inhibition of cyclin-dependent kinase (CDK) is a conserved downstream effect of DNA damage checkpoint signaling pathways in eukaryotes. This role in the regulation of cell proliferation and prevention of cancer has made CDK a leading target for rational drug design and chemotherapy. It is possible that <italic>S. cerevisiae</italic> CDK, Cdc28, may similarly respond to checkpoint signals, though currently no such Cdc28 function has been described. In this work, 6 point mutations in the <italic>CDC28</italic> gene were isolated that confer DNA damage checkpoint defects. Homology modeling of the <italic>CDC28 </italic> describes a putative N-terminal binding site that may function in this pathway.

ISBN: 0493525300Subjects--Topical Terms:

1017686
Biology, Cell.

The G1 DNA damage checkpoint in Saccharomyces cerevisiae.
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245 1 0 $a The G1 DNA damage checkpoint in Saccharomyces cerevisiae.
300 $a 160 p.
500 $a Adviser: Stephen J. Kron.
500 $a Source: Dissertation Abstracts International, Volume: 63-01, Section: B, page: 0030.
502 $a Thesis (Ph.D.)--The University of Chicago, 2002.
520 $a Inhibition of cyclin-dependent kinase (CDK) is a conserved downstream effect of DNA damage checkpoint signaling pathways in eukaryotes. This role in the regulation of cell proliferation and prevention of cancer has made CDK a leading target for rational drug design and chemotherapy. It is possible that <italic>S. cerevisiae</italic> CDK, Cdc28, may similarly respond to checkpoint signals, though currently no such Cdc28 function has been described. In this work, 6 point mutations in the <italic>CDC28</italic> gene were isolated that confer DNA damage checkpoint defects. Homology modeling of the <italic>CDC28 </italic> describes a putative N-terminal binding site that may function in this pathway.
520 $a In these studies it was noticed that 40% of asynchronous wild-type yeast arrest as unbudded cells after 1600 Gy gamma irradiation. This suggests the existence of a novel G1 DNA damage checkpoint. DNA damage in G1 was found to delay onset of replication, bud emergence and spindle pole body duplication and to extend the window of sensitivity to the yeast mating pheromone. These findings all argue that DNA damage can inhibit the Start event in the yeast cell cycle. This G1 arrest is dose-dependent and requires the DNA damage detector <italic> RAD9</italic>, but not the DNA polymerase <italic>POL</italic>ϵ. Whether induced by lethal γ or UV irradiation, the <italic>RAD9</italic>- and <italic> RAD17</italic>-dependent G1 checkpoint arrest can be maintained over 18 hours. Sub-lethal γ irradiation causes haploid yeast to preferentially arrest in G1. This G1 arrest after γ irradiation is prolonged by defects in double-strand break repair, but UV irradiation requires excision repair to initiate an arrest. These results are consistent with single-strand DNA being the initiating signal of checkpoint arrest in G1. The molecular components of the G1 DNA damage checkpoint may provide novel targets for future chemotherapies in the treatment of cancer.
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