Analysis of Gene Targeting & Nonhomologous End-joining. Final Report

Haber, J. E.

Brandeis University, Waltham, Massachusetts (United States)

关键词: Repair;    Dna Damages;    Chromosomes;    Genes;    Telomeres;   

DOI  :  10.2172/825003
RP-ID  :  DOE/ER/9962729
RP-ID  :  FG02-99ER62729
RP-ID  :  825003

美国|英语

来源: UNT Digital Library

【 摘 要 】

Overall, we identified a number of new proteins that participate in nonhomologous end-joining and also in telomere addition to the ends of broken chromosomes. We showed that NHEJ is severely reduced in cells expressing both yeast mating-type genes and then went on to identify the NEJ1 gene that was under this control. We showed the epistasis relations among a set of mutations that impair telomere addition and we showed that there are in fact two pathways to repair broken chromosomes in the absence of telomerase. We characterized the DNA damage checkpoint pathway in response to a single broken chromosome and characterized especially the adaptation of cells arrested by an unrepaired DSB. We demonstrated that the DNA damage response is nuclear-limited. We showed adaptation defects for Tid1and Srs2 proteins and showed that Srs2 was also recovery-defective, even when DNA was repaired.