Submitted on November 28, 2008
Revised on May 29, 2009
Accepted on May 31, 2009
QTL for several metabolic traits map to loci controlling growth and body composition in an F2 inter-cross between high- and low-growth chicken lines
Javad Nadaf1, Frédérique Pitel1, Hélène Gilbert1, Michel J. Duclos2, Florence Vignoles1, Catherine Beaumont1, Alain Vignal1, Tom E. Porter3, Larry A. Cogburn4, Samuel E Aggrey5, Jean Simon6, and Elisabeth Le Bihan-Duval1*
1 INRA
2 Centre de Recherches de Tours
3 University of Maryland
4 University of Delaware
5 University of Georgia
6 INRA-SRA
* To whom correspondence should be addressed. E-mail: lebihan{at}tours.inra.fr.
QTL for metabolic and body composition traits were mapped at 7 and 9 weeks, respectively in an F2 inter-cross between high-growth (HG) and low-growth (LG) chicken lines. These lines also diverged for: abdominal fat percentage (AFP), plasma insulin-like growth factor-1 (IGF-1), insulin and glucose levels. Genotypings were performed using 129 microsatellite markers covering 21 chromosomes. A total of 21 QTL with genome-wide level of significance were detected by single trait (ST) analyses for: body weight (BW), breast muscle weight (BMW) and percentage (BMP), AF weight (AFW) and percentage (AFP), shank length (ShL) and diameter (ShD), fasting plasma glucose level (Gluc) and body temperature (Tb). Other suggestive QTL were identified for these parameters and for plasma IGF-1 and NEFA levels. QTL controlling adiposity and Gluc were co-localized on GGA3 and GGA5 and QTL for BW, shank measurements, adiposity and Tb on GGA4. Multi-trait (MT) analyses revealed two QTL controlling Gluc and AFP on GGA5, and Gluc and Tb on GGA26. Significant effects of the reciprocal cross were observed on BW, ShD, BMW and Gluc, which may result from mtDNA and/or maternal effects. Most QTL regions for Gluc and adiposity harbor genes for which alleles have been associated with increased susceptibility to diabetes and/or obesity in humans. Identification of genes responsible for these metabolic QTL will increase our understanding of the constitutive "hyperglycemia" found in chickens. Furthermore, a comparative approach could provide new information on the genetic causes of diabetes and obesity in humans.
