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• W2158609529 endingPage "11088" @default.
• W2158609529 startingPage "11073" @default.
• W2158609529 abstract "Telomere length is controlled by a homeostatic mechanism that involves telomerase, telomere-associated proteins, and conventional replication machinery. Specifically, the coordinated actions of the lagging strand synthesis and telomerase have been argued. Although DNA polymerase α, an enzyme important for the lagging strand synthesis, has been indicated to function in telomere metabolism in yeasts and ciliates, it has not been characterized in higher eukaryotes. Here, we investigated the impact of compromised polymerase α activity on telomeres, using tsFT20 mouse mutant cells harboring a temperature-sensitive polymerase α mutant allele. When polymerase α was temperature-inducibly inactivated, we observed sequential events that included an initial extension of the G-tail followed by a marked increase in the overall telomere length occurring in telomerase-independent and -dependent manners, respectively. These alterations of telomeric DNA were accompanied by alterations of telomeric chromatin structures as revealed by quantitative chromatin immunoprecipitation and immunofluorescence analyses of TRF1 and POT1. Unexpectedly, polymerase α inhibition resulted in a significantly high incidence of Robertsonian chromosome fusions without noticeable increases in other types of chromosomal aberrations. These results indicate that although DNA polymerase α is essential for genome-wide DNA replication, hypomorphic activity leads to a rather specific spectrum of chromosomal abnormality." @default.
• W2158609529 created "2016-06-24" @default.
• W2158609529 creator A5006788556 @default.
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• W2158609529 creator A5061154995 @default.
• W2158609529 date "2005-12-01" @default.
• W2158609529 modified "2023-10-01" @default.
• W2158609529 title "Alterations of DNA and Chromatin Structures at Telomeres and Genetic Instability in Mouse Cells Defective in DNA Polymerase α" @default.
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• W2158609529 doi "https://doi.org/10.1128/mcb.25.24.11073-11088.2005" @default.
• W2158609529 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1316980" @default.
• W2158609529 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16314528" @default.
• W2158609529 hasPublicationYear "2005" @default.
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