Replication and protection of telomeres

被引:372
作者
Verdun, Ramiro E. [1 ]
Karlseder, Jan [1 ]
机构
[1] Salk Inst Biol Studies, La Jolla, CA 92037 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/nature05976
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
During the evolution of linear genomes, it became essential to protect the natural chromosome ends to prevent triggering of the DNA-damage repair machinery and enzymatic attack. Telomeres - tightly regulated complexes consisting of repetitive G-rich DNA and specialized proteins - accomplish this task. Telomeres not only conceal linear chromosome ends from detection and inappropriate repair but also provide a buffer to counteract replication-associated shortening. Lessons from many model organisms have taught us about the complications of maintaining these specialized structures. Here, we discuss how telomeres interact and cooperate with the DNA replication and DNA-damage repair machineries.
引用
收藏
页码:924 / 931
页数:8
相关论文
共 100 条
[1]   A critical role for telomeres in suppressing and facilitating carcinogenesis [J].
Artandi, SE ;
DePinho, RA .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2000, 10 (01) :39-46
[2]   Frequent recombination in telomeric DNA may extend the proliferative life of telomerase-negative cells [J].
Bailey, SM ;
Brenneman, MA ;
Goodwin, EH .
NUCLEIC ACIDS RESEARCH, 2004, 32 (12) :3743-3751
[3]   Pot1, the putative telomere end-binding protein in fission yeast and humans [J].
Baumann, P ;
Cech, TR .
SCIENCE, 2001, 292 (5519) :1171-1175
[4]  
Bechter OE, 2004, CELL CYCLE, V3, P547
[5]   Delivery of yeast telomerase to a DNA break depends on the recruitment functions of Cdc13 and Est1 [J].
Bianchi, A ;
Negrini, S ;
Shore, D .
MOLECULAR CELL, 2004, 16 (01) :139-146
[6]   Telomere shortening and tumor formation by mouse cells lacking telomerase RNA [J].
Blasco, MA ;
Lee, HW ;
Hande, MP ;
Samper, E ;
Lansdorp, PM ;
DePinho, RA ;
Greider, CW .
CELL, 1997, 91 (01) :25-34
[7]   Extension of life-span by introduction of telomerase into normal human cells [J].
Bodnar, AG ;
Ouellette, M ;
Frolkis, M ;
Holt, SE ;
Chiu, CP ;
Morin, GB ;
Harley, CB ;
Shay, JW ;
Lichtsteiner, S ;
Wright, WE .
SCIENCE, 1998, 279 (5349) :349-352
[8]   Quantitative amplification of single-stranded DNA (QAOS) demonstrates that cdc13-1 mutants generate ssDNA in a telomere to centromere direction [J].
Booth, C ;
Griffith, E ;
Brady, G ;
Lydall, D .
NUCLEIC ACIDS RESEARCH, 2001, 29 (21) :4414-4422
[9]   The Mre11 complex is required for ATM activation and the G2/M checkpoint [J].
Carson, CT ;
Schwartz, RA ;
Stracker, TH ;
Lilley, CE ;
Lee, DV ;
Weitzman, MD .
EMBO JOURNAL, 2003, 22 (24) :6610-6620
[10]   DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion [J].
Celli, GB ;
de Lange, T .
NATURE CELL BIOLOGY, 2005, 7 (07) :712-U110