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生命科学与生物工程学院学术报告

发布日期:2017-4-10 15:27:51      作者:      来源:




报告题目:Genome-Wide Histone Acetylation and theDNA Damage Response



报告人:Professor Alain Verreault


Institute for Research in Immunologyand Cancer (IRIC), Univ. Montreal, Canada


https://www.iric.ca/en/research/principal-investigators/alain-verreault/


alain.verreault@umontreal.ca



报告时间与地点:2017419日13:00至14:30,生命学院理科楼B307室



报告摘要:Abstract


Numerous DNA lesionsthat occur spontaneously and DNA lesions caused by environmental carcinogens orcancer chemotherapeutic agents interfere with the completion of DNAreplication. The links between the repair of DNA lesions that impairreplication and chromatin structure are poorly understood. For many years, ourlaboratory has been studying a fascinating feature of the "chromosomecycle". During DNA replication, newly synthesized histones are rapidlydeposited onto nascent DNA to restore chromatin structure. In the budding yeastSaccharomyces cerevisiae, we showed that essentially all the new histone H3molecules deposited throughout the genome are acetylated at lysine 56 (H3-K56).In the absence of persistent DNA lesions, H3-K56 is deacetylated from theentire genome during G2/M phase of the cell cycle. Thus, genome-wide cycles ofH3-K56 acetylation and deacetylation create transient waves of histone acetylationthat sweep throughout the genome during each passage through the cell cycle.Mutant cells that cannot acetylate or deacetylate H3-K56 exhibit persistentspontaneous DNA lesions and are exquisitely sensitive to chemicals that damageDNA during replication. We present several lines of evidence suggesting thatthe acute sensitivity to DNA damage of mutants in which the H3-K56 acetylationcycle is perturbed stems from mitotic segregation of incompletely duplicatedDNA.


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