Identification of quantitative trait loci associated with bone traits and body weight in an F2 resource population of chickens.

Bone fractures at the end of lay are a significant problem in egg-laying strains of hens. The objective of the current study was to identify quantitative trait loci (QTL) associated with bone mineralization and strength in a chicken resource population. Layer (White Leghorn hens) and broiler (Cobb-Cobb roosters) lines were crossed to generate an F2 population of 508 hens over seven hatches, and 26 traits related to bone integrity, including bone mineral density (BMD) and content (BMC), were measured. Genotypes of 120 microsatellite markers on 28 autosomal groups were determined, and interval mapping was conducted to identify QTL regions. Twenty-three tests representing three chromosomal regions (chromosomes 4, 10 and 27) contained significant QTL that surpassed the 5% genome-wise threshold, and 47 tests representing 15 chromosomes identified suggestive QTL that surpassed the 5% chromosome-wise threshold. Although no significant QTL influencing BMD and BMC were detected after adjusting for variation in body weight and egg production, multiple suggestive QTL were found. These results support previous experiments demonstrating an important genetic regulation of bone strength in chickens, but suggest the regulation may be due to the effects of multiple genes that each account for relatively small amounts of variation in bone strength.

Expression of PEG11 and PEG11AS transcripts in normal and callipyge sheep.

BACKGROUND: The callipyge mutation is located within an imprinted gene cluster on ovine chromosome 18. The callipyge trait exhibits polar overdominant inheritance due to the fact that only heterozygotes inheriting a mutant paternal allele (paternal heterozygotes) have a phenotype of muscle hypertrophy, reduced fat and a more compact skeleton. The mutation is a single A to G transition in an intergenic region that results in the increased expression of several genes within the imprinted cluster without changing their parent-of-origin allele-specific expression. RESULTS: There was a significant effect of genotype (p < 0.0001) on the transcript abundance of DLK1, PEG11, and MEG8 in the muscles of lambs with the callipyge allele. DLK1 and PEG11 transcript levels were elevated in the hypertrophied muscles of paternal heterozygous animals relative to animals of the other three genotypes. The PEG11 locus produces a single 6.5 kb transcript and two smaller antisense strand transcripts, referred to as PEG11AS, in skeletal muscle. PEG11AS transcripts were detectable over a 5.5 kb region beginning 1.2 kb upstream of the PEG11 start codon and spanning the entire open reading frame. Analysis of PEG11 expression by quantitative PCR shows a 200-fold induction in the hypertrophied muscles of paternal heterozygous animals and a 13-fold induction in homozygous callipyge animals. PEG11 transcripts were 14-fold more abundant than PEG11AS transcripts in the gluteus medius of paternal heterozygous animals. PEG11AS transcripts were expressed at higher levels than PEG11 transcripts in the gluteus medius of animals of the other three genotypes. CONCLUSIONS: The effect of the callipyge mutation has been to alter the expression of DLK1, GTL2, PEG11 and MEG8 in the hypertrophied skeletal muscles. Transcript abundance of DLK1 and PEG11 was highest in paternal heterozygous animals and exhibited polar overdominant gene expression patterns; therefore, both genes are candidates for causing skeletal muscle hypertrophy. There was unique relationship of PEG11 and PEG11AS transcript abundance in the paternal heterozygous animals that suggests a RNA interference mechanism may have a role in PEG11 gene regulation and polar overdominance in callipyge sheep.

Altered mRNA abundance of ASB15 and four other genes in skeletal muscle following administration of beta-adrenergic receptor agonists.

Beta-adrenergic receptor agonists (BA) stimulate skeletal muscle growth. However, downstream signaling pathways that facilitate this effect remain poorly defined. Objectives of this study were to identify genes differentially expressed after administration of a novel BA and to evaluate the expression of one of those genes in additional models of skeletal muscle growth. Differentially expressed gene fragments were identified through differential display of skeletal muscle biopsies from five steers 24 h after administration of the BA. Five gene fragments designated DD53, DD143, DD163, DD209, and DD214 were identified. Tissue distribution of these genes was evaluated by RT-PCR. While DD53, DD163, DD209, and DD214 were expressed across tissues, DD143 mRNA expression was most abundant in skeletal muscle. DD143, later identified as bovine ASB15, was evaluated in rats following administration of anabolic compounds. Thirteen 7-wk-old female rats were randomly assigned to each of four treatment groups including: control, clenbuterol, trenbolone acetate (TBA), and growth hormone (GH). Changes in rat Asb-15 mRNA were measured at 30 min, 12 h, and 24 h following intraperitoneal injections of each compound. Clenbuterol treatment decreased Asb-15 mRNA in skeletal muscle at 12 and 24 h (P < 0.01) and also decreased mRNA in lung at 12 h (P < 0.05). TBA and GH treatments did not alter Asb-15 mRNA in any of the tissues evaluated (P > 0.10). These results are the first to associate an Asb gene family member with muscle growth or BA administration and suggest a potential role for ASB15 in beta-agonist-induced skeletal muscle hypertrophy.