trt-1 is the Caenorhabditis elegans catalytic subunit of telomerase.
trt-1 is the Caenorhabditis elegans catalytic subunit of telomerase.
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TRT-1是秀丽隐杆线虫催化亚基的端粒酶。
DOI：
10.1371/journal.pgen.0020018
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发表时间：
2006-02
期刊：
影响因子：
4.5
通讯作者：
Ahmed, Shawn
中科院分区：
文献类型：
--
作者：
Meier, Bettina;Clejan, Iuval;Liu, Yan;Lowden, Mia;Gartner, Anton;Hodgkin, Jonathan;Ahmed, Shawn
突变体的trt-1，秀丽隐杆线虫端粒酶逆转录酶，正常繁殖几代，但最终成为不育的端粒侵蚀和端到端的染色体融合的结果。端粒侵蚀和脱帽不会导致trt-1突变体种系细胞凋亡的增加。相反，晚一代的trt-1突变体显示染色体分离缺陷，这可能是不育的直接原因。trt-1在与mrt-2相同的端粒复制途径中起作用，mrt-2是Rad 9/Rad 1/Hus 1（9-1-1）增殖细胞核抗原样滑动夹的组分。因此，9-1-1复合物可能是端粒酶在C染色体末端起作用所必需的。优雅的。虽然端粒的破坏限制了人类体细胞的复制寿命，但trt-1和端粒缩短都不影响C.优雅的。这些发现说明了C中端粒功能障碍的影响。缺乏端粒酶催化亚单位TRT-1的线虫突变体。 在20世纪30年代，玉米遗传学家芭芭拉·麦克林托克（Barbara McClintock）观察到，断裂的染色体末端偶尔会在通过生殖系传递时变得稳定，她推断，正常染色体末端的保护帽可以重新添加到断裂的染色体上。我们现在知道，在大多数真核生物中，短的重复DNA序列覆盖染色体末端，并且这种序列可以通过端粒酶逆转录酶从头添加，端粒酶逆转录酶使用RNA模板进行端粒重复添加。作者从遗传学上定义了秀丽隐杆线虫中端粒酶的逆转录酶亚基。对异常DNA损伤作出反应的蛋白质是C.这表明染色体末端可能被认为是一种特殊形式的DNA损伤之前，端粒重复添加端粒酶。作者发现，端粒酶和DNA损伤反应蛋白似乎在相同的端粒复制途径中起作用。人类体细胞的复制性衰老可能是由端粒缩短引起的。然而，体细胞在C中不增殖。在这种情况下，端粒侵蚀不会影响衰老过程。最后，作者观察到染色体错误分离可能解释了C.线虫端粒酶突变体
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. In the 1930s, the maize geneticist Barbara McClintock observed that broken chromosome ends occasionally became stable when transmitted through the germline, and she inferred that a protective cap present at normal chromosome ends could be added to broken chromosomes de novo. We now know that short, repetitive DNA sequences cap chromosome ends in most eukaryotes and that such sequences can be added de novo by the telomerase reverse transcriptase, which uses an RNA template for telomere repeat addition. The authors genetically define the reverse transcriptase subunit of telomerase in the roundworm Caenorhabditis elegans. Proteins that respond to abnormal DNA damage are required for telomere replication in C. elegans, suggesting that chromosome ends may be recognized as a special form of DNA damage prior to telomere repeat addition by telomerase. The authors found that telomerase and DNA damage response proteins appear to function in the same telomere replication pathway. Replicative aging in human somatic cells may be caused by telomere shortening. However, somatic cells do not proliferate in C. elegans adults, and telomere erosion does not affect the aging process in this context. Finally, the authors observed that chromosome mis-segregation may explain the progressive sterility of C. elegans telomerase mutants.
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