An F2 chicken population was established from a cross of a broiler sire-line and an egg laying (White Leghorn) line. There were two males and two females from both lines in the base population. The F1 progeny consisted of 8 males and 32 females. Over 500 F2 offspring from five hatches were reared to slaughter at a live weight of 2 kg at 9 wk of age. Body weights at 3, 6, and 9 wk were recorded. The DNA was extracted from blood samples, and genotypes for 101 microsatellite markers were determined. Data of 466 individuals from 30 families were available for analysis. Interval mapping QTL analyses were carried out. The QTL significant at the genome wide level that affected body weight at two ages were identified on chromosomes 1, 2, 4, 7, and 8 and a QTL on Chromosome 13 influenced body weight at all three ages. Genetic effects were generally additive, and the broiler allele increased body weight in all cases. The effects for significant individual QTL accounted for between 0.2 and 1.0 phenotypic standard deviations and the sum of the additive effects accounted for approximately 0.75 of the line difference in body weight at 6 wk of age. The largest single additive effect was on chromosome 4, and the effect of substituting one copy of the gene was an increase in weight of 249 g. Interactions of the QTL with sex or family were unimportant. There was no evidence for imprinting or of two or more QTL at the same location for any of the traits.

An F2 chicken population of 442 individuals from 30 families, obtained by crossing a broiler line with a layer line, was used for detecting and mapping Quantitative Trait Loci (QTL) affecting abdominal fat weight, skin fat weight and fat distribution. Within-family regression analyses using 102 microsatellite markers in 27 linkage groups were carried out with genome-wide significance thresholds. The QTL for abdominal fat weight were found on chromosomes 3, 7, 15 and 28; abdominal fat weight adjusted for carcass weight on chromosomes 1, 5, 7 and 28; skin and subcutaneous fat on chromosomes 3, 7 and 13; skin fat weight adjusted for carcass weight on chromosomes 3 and 28; and skin fat weight adjusted for abdominal fat weight on chromosomes 5, 7 and 15. Interactions of the QTL with sex or family were unimportant and, for each trait, there was no evidence for imprinting or of multiple QTL on any chromosome. Significant dominance effects were obtained for all but one of the significant locations for QTL affecting the weight of abdominal fat, none for skin fat and one of the three QTL affecting fat distribution. The magnitude of each QTL ranged from 3.0 to 5.2% of the residual phenotypic variation or 0.2-0.8 phenotypic standard deviations. The largest additive QTL (on chromosome 7) accounted for more than 20% of the mean weight of abdominal fat. Significant positive and negative QTL were identified from both lines.

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