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TRT-1是秀丽隐杆线虫端粒酶的催化亚基。

trt-1 is the Caenorhabditis elegans catalytic subunit of telomerase.

作者信息

Meier Bettina, Clejan Iuval, Liu Yan, Lowden Mia, Gartner Anton, Hodgkin Jonathan, Ahmed Shawn

机构信息

Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA.

出版信息

PLoS Genet. 2006 Feb;2(2):e18. doi: 10.1371/journal.pgen.0020018. Epub 2006 Feb 10.

Abstract

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.

摘要

秀丽隐杆线虫端粒酶逆转录酶trt-1的突变体在几代内能够正常繁殖,但最终会因端粒侵蚀和染色体端对端融合而变得不育。端粒侵蚀和去帽不会导致trt-1突变体生殖系中细胞凋亡增加。相反,晚期trt-1突变体表现出染色体分离缺陷,这可能是不育的直接原因。trt-1与mrt-2在相同的端粒复制途径中发挥作用,mrt-2是Rad9/Rad1/Hus1(9-1-1)增殖细胞核抗原样滑动夹的一个组成部分。因此,9-1-1复合物可能是端粒酶在秀丽隐杆线虫染色体末端发挥作用所必需的。虽然端粒侵蚀限制了人类体细胞的复制寿命,但trt-1和端粒缩短都不会影响秀丽隐杆线虫的有丝分裂后衰老。这些发现说明了缺乏端粒酶催化亚基trt-1的秀丽隐杆线虫突变体中端粒功能障碍的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0530/1378126/ac0002bf1fb3/pgen.0020018.g001.jpg

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