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短端粒在酿酒酵母中诱导DNA损伤反应。

Short telomeres induce a DNA damage response in Saccharomyces cerevisiae.

作者信息

IJpma Arne S, Greider Carol W

机构信息

Department of Molecular Biology and Genetics, Graduate Program in Cellular and Molecular Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

出版信息

Mol Biol Cell. 2003 Mar;14(3):987-1001. doi: 10.1091/mbc.02-04-0057.

Abstract

Telomerase-deficient Saccharomyces cerevisiae cells show a progressive decrease in telomere length. When grown for several days in log phase, the tlc1Delta cells initially display wild-type growth kinetics with subsequent loss of growth potential after which survivors are generated via RAD52-dependent homologous recombination. We found that chromosome loss in these telomerase-deficient cells only increased after a significant decline in growth potential of the culture. At earlier stages of growth, as the telomerase-deficient cells began to show loss of growth potential, the cells arrested in G2/M and showed RNR3 induction and Rad53p phosphorylation. These responses were dependent on RAD24 and MEC1, suggesting that short telomeres are recognized as DNA damage and signal G2/M arrest.

摘要

端粒酶缺陷型酿酒酵母细胞的端粒长度呈现出逐渐下降的趋势。当在对数生长期培养数天时,tlc1Delta细胞最初表现出野生型的生长动力学,随后生长潜力丧失,之后通过RAD52依赖的同源重组产生存活细胞。我们发现,在这些端粒酶缺陷型细胞中,染色体丢失仅在培养物生长潜力显著下降后才增加。在生长的早期阶段,随着端粒酶缺陷型细胞开始表现出生长潜力丧失,细胞停滞在G2/M期,并表现出RNR3诱导和Rad53p磷酸化。这些反应依赖于RAD24和MEC1,表明短端粒被识别为DNA损伤并引发G2/M期停滞。

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