A novel role of peroxin PEX6: Suppression of aging defects in mitochondria

Jae Gu Seo, Chi-Yung Lai, Michael V. Miceli, S. Michal Jazwinski

研究成果: Article

26 引文 斯高帕斯(Scopus)

摘要

Yeast cells become older with each division, but their daughters are born young. Mutational analysis shows that maintenance of this age asymmetry requires segregation of a complement of active mitochondria to daughters and that this process breaks down in older mother cells. This decline has implications for stem cell aging in higher organisms. PEX6, a peroxisome biogenesis gene, has been isolated as a multicopy suppressor of an atp2 age asymmetry mutant. Suppression depended on the presence of particular amino acid residues in Atp2p, and required adenosine triphosphate (ATP) binding and/or ATP hydrolysis activity of Pex6p. Extra copies of PEX6 corrected the deficit in Atp2p in mitochondria in the mutant by improving its import kinetics, resulting in near normal mitochondrial inheritance by daughter cells. The novel function of Pex6p described here may provide insights into peroxisomal and mitochondrial disorders and into metabolic diseases in general.

原文English
頁(從 - 到)405-413
頁數9
期刊Aging Cell
6
發行號3
DOIs
出版狀態Published - 2007 六月 1

    指紋

All Science Journal Classification (ASJC) codes

  • Ageing
  • Cell Biology

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