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嗜热栖热菌:一种用于研究健康衰老机制的模式生物。

Podospora anserina: a model organism to study mechanisms of healthy ageing.

作者信息

Scheckhuber Christian Q, Osiewacz Heinz D

机构信息

Cluster of Excellence Macromolecular Complexes and Faculty for Biosciences, Molecular Developmental Biology, Johann Wolfgang Goethe University, Max-von-Laue-Str. 9, 60438, Frankfurt/Main, Germany.

出版信息

Mol Genet Genomics. 2008 Nov;280(5):365-74. doi: 10.1007/s00438-008-0378-6. Epub 2008 Sep 17.

DOI:10.1007/s00438-008-0378-6
PMID:18797929
Abstract

The filamentous ascomycete Podospora anserina has been extensively studied as an experimental ageing model for more than 50 years. As a result, a huge body of data has been accumulated and various molecular pathways have been identified as part of a molecular network involved in the control of ageing and life span. The aim of this review is to summarize data on P. anserina ageing, including aspects like respiration, cellular copper homeostasis, mitochondrial DNA (mtDNA) stability/instability, mitochondrial dynamics, apoptosis, translation efficiency and pathways directed against oxidative stress. It becomes clear that manipulation of several of these pathways bears the potential to extend the healthy period of time, the health span, within the life time of the fungus. Here we put special attention on recent work aimed to identify and characterize this type of long-lived P. anserina mutants. The study of the molecular pathways which are modified in these mutants can be expected to provide important clues for the elucidation of the mechanistic basis of this type of 'healthy ageing' at the organism level.

摘要

丝状子囊菌嗜热栖热孢霉作为实验性衰老模型已被广泛研究了50多年。因此,积累了大量数据,并确定了各种分子途径,作为参与衰老和寿命控制的分子网络的一部分。本综述的目的是总结嗜热栖热孢霉衰老的数据,包括呼吸、细胞铜稳态、线粒体DNA(mtDNA)稳定性/不稳定性、线粒体动力学、细胞凋亡、翻译效率以及针对氧化应激的途径等方面。很明显,对这些途径中的几个进行调控有可能延长真菌生命周期内的健康时间,即健康寿命。在此,我们特别关注旨在鉴定和表征这种长寿嗜热栖热孢霉突变体的近期研究工作。预计对这些突变体中发生改变的分子途径的研究将为阐明生物体水平上这种“健康衰老”的机制基础提供重要线索。

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Simultaneous Ablation of the Catalytic AMPK α-Subunit SNF1 and Mitochondrial Matrix Protease CLPP Results in Pronounced Lifespan Extension.同时敲除催化性AMPKα亚基SNF1和线粒体基质蛋白酶CLPP可显著延长寿命。
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Quercetin-Induced Lifespan Extension in Requires Methylation of the Flavonoid by the -Methyltransferase PaMTH1.槲皮素诱导的[具体生物]寿命延长需要黄酮类化合物由甲基转移酶PaMTH1进行甲基化。 (注:原文中“in ”后面缺少具体生物名称)
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