Gene expression profiling implicates OXPHOS complexes in lifespan extension of flies over-expressing a small mitochondrial chaperone, Hsp22.

Authors: Kim HJ; Morrow G; Westwood JT; Michaud S; Tanguay RM
Year: 2010
Journal: Experimental gerontology
Abstract: Aging is a complex process accompanied by a decreased capacity to tolerate and respond to various stresses. Heat shock proteins as part of cell defense mechanisms are up-regulated following stress. In Drosophila, the mitochondrial Hsp22 is preferentially up-regulated in aged flies. Its over-expression results in an extension of lifespan and an increased resistance to stress. Hsp22 has chaperone-like activity in vitro, but the mechanism(s) by which it increases lifespan in flies are unknown. Genome-wide analysis was performed on long-lived Hsp22+ and control flies to unveil transcriptional changes brought by Hsp22. Transcriptomes obtained at 45days, 90% and 50% survival were then compared between them to focus more on genes up- or down-regulated in presence of higher levels of hsp22 mRNA. Hsp22+ flies display an up-regulation of genes mainly related to mitochondrial energy production and protein biosynthesis, two functions normally down-regulated during aging. Interestingly, among the 26 genes up-regulated in Hsp22+ flies, 7 genes encode for mitochondrial proteins, 5 of which being involved in OXPHOS complexes. Other genes that could influence aging such as CG5002, dGCC185 and GstS1 also displayed a regulation linked to Hsp22 expression. The up-regulation of genes of the OXPHOS system in Hsp22+ flies suggest that mitochondrial homeostasis is at the center of Hsp22 beneficial effects on lifespan.
Reference

Integration:

Created on Nov. 5, 2012, 6:24 p.m.
Not linked
Integrated: False

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Species: Fruit fly

Experiments: 0
Interventions:
  • Hsp22 transposition
  • Hsp22 overexpression

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