The identities of genes that underlie population variation in adipose tissue development in farm animals are poorly understood. Previous studies in our laboratory have suggested that increased fat tissue involves the expression modulation of an array of genes in broiler chickens. Of special interest are eight genes, FGFR3, EPHB2, IGFBP2, GREM1, TNC, COL3A1, ACBD7, and SCD. To understand their expression regulation and response to dietary manipulation, we investigated their mRNA levels after dietary manipulation during early development. Chickens were fed either a recommended standard or a high caloric diet from hatch to eight weeks of age (WOA). The high caloric diet markedly affected bodyweight of the broiler birds. mRNA levels of the eight genes in the abdominal adipose tissue were assayed at 2, 4, 6, and 8 WOA using RT-qPCR. Results indicate that (1) FGFR3 mRNA level was affected significantly by diet, age, and diet:age interaction; (2) COL3A mRNA level was repressed by high caloric diet; (3) mRNA levels of EPHB2, ACBD7, and SCD were affected by age; (4) mRNA level of TNC was modulated by age:diet interaction; (5) changes in GREM1 and IGFBP2 mRNA levels were not statistically different. 1. Introduction In chickens, quantitative trait loci (QTL) mapping studies have identified a number of loci in fat deposition [1–7]. In different mapping populations, the loci that contribute to fat deposition appear to be unique because different chicken strains inherited a unique set of alleles. Since QTL mapping studies are often conducted in F2 crosses or backcrosses, which have limited chromosomal crossovers, they often end up with broad chromosomal regions in which hundreds of candidate genes may potentially be responsible for the fat QTL. The identities of genes or regulatory elements for the inferred traits are thus unknown. On the other hand, candidate genes are often evaluated through association studies using DNA sequence variations such as single nucleotide polymorphism (SNP) and short tandem repeats [8–12]. Various alleles of quite a few of the evaluated genes were shown to increase fat deposition. During early development, the chicken adipose tissue grows by both hyperplasia and hypertrophy [13, 14]. Hyperplasia depends on the proliferation of preadipocytes, since mature adipocytes do not multiply. Although there are few studies on preadipocyte proliferation in chickens [15–19], it is generally believed that its mechanism would be similar to that in mammals and other vertebrates, as almost all genes that play key roles in mammals are also found in the
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