Open AccessA novel role of peroxin PEX6 : suppression of aging defects in mitochondria
Author(s) -
Seo JaeGu,
Lai ChiYung,
Miceli Michael V.,
Jazwinski S. Michal
Publication year - 2007
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2007.00291.x
Subject(s) - biology , mitochondrion , mutant , peroxisome , adenosine triphosphate , microbiology and biotechnology , mitochondrial biogenesis , biogenesis , non mendelian inheritance , cell division , genetics , yeast , biochemistry , gene , mitochondrial dna , cell
Summary 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.