Genomic Instability and Cellular Senescence: Lessons From the Budding Yeast

被引:13
|
作者
Lee, Jee Whu [1 ,2 ]
Ong, Eugene Boon Beng [1 ,2 ]
机构
[1] Univ Sains Malaysia, Inst Res Mol Med INFORMM, George Town, Malaysia
[2] Univ Sains Malaysia, USM RIKEN Int Ctr Aging Sci URICAS, George Town, Malaysia
关键词
aging; longevity; rDNA stability; Saccharomyces cerevisiae; senescence; telomere length homeostasis; QUADRUPLEX-PROMOTING ACTIVITY; BREAK-INDUCED REPLICATION; DNA-POLYMERASE-EPSILON; RIBOSOMAL-RNA GENE; SACCHAROMYCES-CEREVISIAE; TELOMERE LENGTH; LIFE-SPAN; UNPROTECTED TELOMERES; BINDING-PROTEIN; END PROTECTION;
D O I
10.3389/fcell.2020.619126
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Aging is a complex biological process that occurs in all living organisms. Aging is initiated by the gradual accumulation of biomolecular damage in cells leading to the loss of cellular function and ultimately death. Cellular senescence is one such pathway that leads to aging. The accumulation of nucleic acid damage and genetic alterations that activate permanent cell-cycle arrest triggers the process of senescence. Cellular senescence can result from telomere erosion and ribosomal DNA instability. In this review, we summarize the molecular mechanisms of telomere length homeostasis and ribosomal DNA stability, and describe how these mechanisms are linked to cellular senescence and longevity through lessons learned from budding yeast.
引用
收藏
页数:9
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