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First published online April 18, 2008
Journal of Experimental Biology 211, 1448-1455 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.014951

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Role of the PGC-1 family in the metabolic adaptation of goldfish to diet and temperature

Christophe M. R. LeMoine, Christine E. Genge and Christopher D. Moyes^*

Department of Biology, Queen's University, Kingston, ON K7L 3N6, Canada

^* Author for correspondence (e-mail: chris.moyes{at}queensu.ca)

Accepted 4 March 2008

In mammals, the peroxisome proliferator-activated receptor (PPAR) coactivator-1 (PGC-1) family members and their binding partners orchestrate remodelling in response to diverse challenges such as diet, temperature and exercise. In this study, we exposed goldfish to three temperatures (4, 20 and 35°C) and to three dietary regimes (food deprivation, low fat and high fat) and examined the changes in mitochondrial enzyme activities and transcript levels for metabolic enzymes and their genetic regulators in red muscle, white muscle, heart and liver. When all tissues and conditions were pooled, there were significant correlations between the mRNA for the PGC-1 coactivators (both and β) and mitochondrial transcripts (citrate synthase), metabolic gene regulators including PPAR, PPARβ and nuclear respiratory factor-1 (NRF-1). PGC-1β was the better predictor of the NRF-1 axis, whereas PGC-1 was the better predictor of the PPAR axis (PPAR, PPARβ, medium chain acyl CoA dehydrogenase). In contrast to these intertissue/developmental patterns, the response of individual tissues to physiological stressors displayed no correlations between mRNA for PGC-1 family members and either the NRF-1 or PPAR axes. For example, in skeletal muscles, low temperature decreased PGC-1 transcript levels but increased mitochondrial enzyme activities (citrate synthase and cytochrome oxidase) and transcripts for COX IV and NRF-1. These results suggest that in goldfish, as in mammals, there is a regulatory relationship between (i) NRF-1 and mitochondrial gene expression and (ii) PPARs and fatty acid oxidation gene expression. In contrast to mammals, there is a divergence in the roles of the coactivators, with PGC-1 linked to fatty acid oxidation through PPAR, and PGC-1β with a more prominent role in mediating NRF-1-dependent control of mitochondrial gene expression, as well as distinctions between their respective roles in development and physiological responsiveness.

Key words: PPAR, NRF-1, mitochondria, transcriptional regulation

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