期刊
PLOS GENETICS
卷 2, 期 2, 页码 187-197出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.0020018
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资金
- MRC [G0000114] Funding Source: UKRI
- Medical Research Council [G0000114] Funding Source: researchfish
- Medical Research Council [G0000114] Funding Source: Medline
- NIGMS NIH HHS [R56 GM066228, R01 GM066228, GM066228] Funding Source: Medline
Mutants of trt-1, the Caenorhabditis elegans telomerase reverse transcriptase, reproduce normally for several generations but eventually become sterile as a consequence of telomere erosion and end-to-end chromosome fusions. Telomere erosion and uncapping do not cause an increase in apoptosis in the germlines of trt-1 mutants. Instead, late-generation trt-1 mutants display chromosome segregation defects that are likely to be the direct cause of sterility. trt-1 functions in the same telomere replication pathway as mrt-2, a component of the Rad9/Rad1/Hus1 (9-1-1) proliferating cell nuclear antigen - like sliding clamp. Thus, the 9 - 1 - 1 complex may be required for telomerase to act at chromosome ends in C. elegans. Although telomere erosion limits replicative life span in human somatic cells, neither trt-1 nor telomere shortening affects postmitotic aging in C. elegans. These findings illustrate effects of telomere dysfunction in C. elegans mutants lacking the catalytic subunit of telomerase, trt-1.
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