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

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

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)405-413
Number of pages9
JournalAging Cell
Volume6
Issue number3
DOIs
Publication statusPublished - 2007 Jun 1

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Mitochondria
Stem Cells
Adenosine Triphosphate
Peroxisomal Disorders
Mitochondrial Diseases
Peroxisomes
Mitochondrial Genes
Cell Aging
Metabolic Diseases
Hydrolysis
Yeasts
Maintenance
Amino Acids
Genes

All Science Journal Classification (ASJC) codes

  • Ageing
  • Cell Biology

Cite this

Seo, Jae Gu ; Lai, Chi-Yung ; Miceli, Michael V. ; Jazwinski, S. Michal. / A novel role of peroxin PEX6 : Suppression of aging defects in mitochondria. In: Aging Cell. 2007 ; Vol. 6, No. 3. pp. 405-413.
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A novel role of peroxin PEX6 : Suppression of aging defects in mitochondria. / Seo, Jae Gu; Lai, Chi-Yung; Miceli, Michael V.; Jazwinski, S. Michal.

In: Aging Cell, Vol. 6, No. 3, 01.06.2007, p. 405-413.

Research output: Contribution to journalArticle

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