National Changhua University of Education Institutional Repository : Item 987654321/8998

English | 正體中文 | 简体中文 | Items with full text/Total items : 6507/11669
Visitors : 29929157 Online Users : 453

RC Version 3.2 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.

Scope Adv. Search

Login ‧ Upload ‧ Help ‧ About ‧ Administer

NCUEIR > College of Science > biotech > Periodical Articles > Item 987654321/8998

Please use this identifier to cite or link to this item: http://ir.ncue.edu.tw/ir/handle/987654321/8998

Title:	A Novel Role of Peroxin Pex6: Suppression of Aging Defects in Mitochondria
Authors:	Seo, J. G.;C. Y. Lai;M. V. Miceli;S. M. Jazwinski
Contributors:	生物系
Keywords:	Age asymmetry;Aging;Metabolism;Peroxisomes;Stem cells
Date:	2007-06
Issue Date:	2011-05-16T07:39:48Z
Publisher:	Wiley-Blackwell
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.
Relation:	Aging Cell, 6(3):405-413
Appears in Collections:	[biotech] Periodical Articles

Files in This Item:

There are no files associated with this item.