Extended Abstract
Background: Growth rate is among the most economically important traits in broiler chickens that varies according to the bird’s genetic potential while being modulated by non-genetic factors. Ascites syndrome is a metabolic–genetic disorder in broilers whose occurrence is associated with genetic susceptibility and environmental conditions, including feeding strategy and husbandry practices. Historically, its prevalence has shown a direct relationship with increasing altitude above sea level; however, ascites is now observed at low altitudes as well, which is attributed to metabolic constraints rather than hypobaric hypoxia alone. The syndrome is seen predominantly in male broilers. Based on the frequently stated view that faster growth can be accompanied by increased physiological strain, it has been hypothesized that some gene variants implicated in ascites susceptibility might also align with—or even enhance—growth-related traits. The present study aimed to evaluate the association between polymorphisms in two ascites-related candidate genes, PDK4 and THRSP, and weekly body weight as well as growth rate traits in a commercial broiler line.
Methods: The research was conducted in three phases: bioinformatics, farm, and laboratory. In the bioinformatics phase, RNA-seq data were used to identify variants in six genes (CPT1A, GPR182, MEF2A, FABP4, PDK4, and THRSP). A downstream RFLP marker-design step was then implemented to prioritize loci amenable to genotyping with a low-cost restriction enzyme, thereby improving feasibility for population-level screening. Ultimately, one biallelic T/C variant from PDK4 and one biallelic A/G variant from THRSP were selected for empirical evaluation; both loci were genotyped using ScaI. In the farm phase, the study population comprised 823 birds (381 males and 442 females) from 23 sire half-sib families. Body weight was recorded weekly from day 1 through day 42. Growth rate was computed over three intervals: 1–21, 21–42, and
1–42 days of age. Ascitic birds were identified using external characteristics commonly adopted in field settings, including feather ruffling, wing drooping, and the presence of a watery abdominal effusion. Records from 114 chicks partitioned into four groups were used for genotype–phenotype association analyses: healthy males (n = 44), ascitic males (n = 11), healthy females (n = 55), and ascitic females (n = 4). Statistical analyses employed the UNIVARIATE and GLM procedures in SAS. Sex, health status, and genotype were modeled as fixed effects. Post-hoc pairwise comparisons were conducted with Tukey’s test to control for multiple testing across genotype classes and sex–health strata.
Results: Across the six genes surveyed, 75 SNPs were identified, 57 of which were determined to be suitable for genotyping by RFLP using an appropriate restriction enzyme. Following additional filtering for assaying robustness and expected informativeness, one variant from PDK4 and one from THRSP were advanced to laboratory validation and association testing. Both loci displayed sufficient genotypic variability for meaningful analysis. At the PDK4 locus, the frequencies of CC, TC, and TT genotypes were 0.105, 0.658, and 0.237, respectively. At the THRSP locus, the frequencies of AA, AG, and GG genotypes were 0.185, 0.500, and 0.315, respectively. As expected from biological dimorphism in broilers, males exhibited higher body weights and growth rates than females at most ages. In parallel, ascitic birds—particularly toward the end of the growing period—showed reduced growth and weight gain compared to healthy counterparts, reflecting the physiological burden of the syndrome. Despite these consistent population-level trends, no genotype at either locus produced statistically significant differences (P > 0.05) in weekly body weight traits or in growth rates across 1–21, 21–42, and 1–42 days. Model estimates did suggest small, non-significant patterns: for PDK4, mean values for CC were marginally higher than those for TC/TT at certain time points; for THRSP, AA tended to show modestly higher phenotypic values than AG/GG. However, effect sizes were below conventional thresholds for statistical reliability and did not survive multiple-comparison control. These findings are consistent with recent perspectives arguing that reduced cardiopulmonary efficiency, rather than growth rate per se, is the proximate driver of ascites in fast-growing birds. In other words, a simple, direct correlation between alleles that support rapid growth and alleles that predispose to ascites is unlikely to be universal, at least for the two loci examined here.
Conclusion: Taken together, the results indicate that the selected polymorphisms in PDK4 and THRSP are not significantly associated with growth-related traits and weekly body weight in this population. A conservative interpretation is that genetic susceptibility to ascites is not necessarily mediated by the same variants that promote faster growth. Rapid growth, by itself, does not equate to a “genotype predisposed to ascites”; rather, ascites risk appears to be contingent on a mismatch between oxygen-delivery capacity and the metabolic demands imposed by growth and husbandry conditions. In conclusion, the present data provide no evidence of a direct genetic link between rapid growth and ascites susceptibility at the level of the two tested genes. Thus, breeding programs can continue to focus on improving growth and efficiency without a direct,
locus-specific increase in ascites risk from these variants—provided that physiological monitoring and environmental management are maintained to balance oxygen demand with tissue capacity.
Type of Study:
Research |
Subject:
ژنتیک و اصلاح نژاد طیور Received: 2025/02/3 | Accepted: 2025/05/19