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本文引用的文献

1
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.端粒酶重新激活可逆转端粒酶缺陷型老年小鼠的组织退化。
Nature. 2011 Jan 6;469(7328):102-6. doi: 10.1038/nature09603. Epub 2010 Nov 28.
2
The effect of replication initiation on gene amplification in the rDNA and its relationship to aging.复制起始对核糖体DNA基因扩增的影响及其与衰老的关系。
Mol Cell. 2009 Sep 11;35(5):683-93. doi: 10.1016/j.molcel.2009.07.012.
3
Effects of age on meiosis in budding yeast.年龄对芽殖酵母减数分裂的影响。
Dev Cell. 2009 Jun;16(6):844-55. doi: 10.1016/j.devcel.2009.05.013.
4
A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants.长寿秀丽隐杆线虫突变体中的体细胞向种系转化。
Nature. 2009 Jun 25;459(7250):1079-84. doi: 10.1038/nature08106. Epub 2009 Jun 7.
5
Meiosis I is established through division-specific translational control of a cyclin.减数分裂I是通过对一种细胞周期蛋白进行特定于分裂的翻译控制而建立的。
Cell. 2008 Apr 18;133(2):280-91. doi: 10.1016/j.cell.2008.02.032.
6
Dissecting timing variability in yeast meiosis.剖析酵母减数分裂中的时间变异性。
Cell. 2007 Nov 2;131(3):544-56. doi: 10.1016/j.cell.2007.09.044.
7
Chromosome mobility during meiotic prophase in Saccharomyces cerevisiae.酿酒酵母减数分裂前期的染色体移动
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):16934-9. doi: 10.1073/pnas.0704860104. Epub 2007 Oct 15.
8
Accelerated aging and failure to segregate damaged proteins in Sir2 mutants can be suppressed by overproducing the protein aggregation-remodeling factor Hsp104p.Sir2突变体中加速衰老和受损蛋白质无法分离的现象可通过过量表达蛋白质聚集重塑因子Hsp104p来抑制。
Genes Dev. 2007 Oct 1;21(19):2410-21. doi: 10.1101/gad.439307.
9
Ascospore formation in the yeast Saccharomyces cerevisiae.酿酒酵母中子囊孢子的形成。
Microbiol Mol Biol Rev. 2005 Dec;69(4):565-84. doi: 10.1128/MMBR.69.4.565-584.2005.
10
Behaviour of nucleolus organizing regions (NORs) and nucleoli during mitotic and meiotic divisions in budding yeast.芽殖酵母有丝分裂和减数分裂过程中核仁组织区(NORs)和核仁的行为。
Chromosome Res. 2004;12(5):427-38. doi: 10.1023/B:CHRO.0000034726.05374.db.

配子发生消除了年龄引起的细胞损伤,并重置了酵母的寿命。

Gametogenesis eliminates age-induced cellular damage and resets life span in yeast.

机构信息

David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

出版信息

Science. 2011 Jun 24;332(6037):1554-7. doi: 10.1126/science.1204349.

DOI:10.1126/science.1204349
PMID:21700873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3923466/
Abstract

Eukaryotic organisms age, yet detrimental age-associated traits are not passed on to progeny. How life span is reset from one generation to the next is not known. We show that in budding yeast resetting of life span occurs during gametogenesis. Gametes (spores) generated by aged cells show the same replicative potential as gametes generated by young cells. Age-associated damage is no longer detectable in mature gametes. Furthermore, transient induction of a transcription factor essential for later stages of gametogenesis extends the replicative life span of aged cells. Our results indicate that gamete formation brings about rejuvenation by eliminating age-induced cellular damage.

摘要

真核生物会衰老,但有害的与年龄相关的特征不会传递给后代。生命跨度如何从一代重置到下一代尚不清楚。我们表明,在出芽酵母中,寿命的重置发生在配子发生期间。来自衰老细胞的配子(孢子)与来自年轻细胞的配子具有相同的复制潜力。在成熟配子中不再检测到与年龄相关的损伤。此外,短暂诱导对于配子发生后期阶段至关重要的转录因子可延长衰老细胞的复制寿命。我们的结果表明,配子形成通过消除与年龄相关的细胞损伤而带来恢复活力。