Abstract
Modern breeding strategies have engendered pronounced disparities in muscle mass and quality between indigenous chickens and specialized broilers. Despite these observable phenotypic differences, the molecular regulatory mechanisms that underpin these variations remain largely uncharacterized. The objective of this study was to elucidate the key genes and regulatory pathways that govern the differential development of pectoral muscle between indigenous chickens and specialized broilers. The differences in myofiber development between the fast-growing commercial broiler breed Arbor Acres (AA) and the slow-growing local breed Taoyuan chickens (TY) were compared through phenotypic and transcriptome sequencing of pectoral muscle development at multiple time points. Subsequently, functional validation of the differentially expressed genes between the two breeds was performed using chicken primary myoblasts in vitro. In vivo experiments revealed that AA and TY chickens shared certain commonalities in growth and pectoral muscle development, but at the same time, there were also significant differences between them. The data analysis of the pectoral muscle transcriptome identified that DUSP1 may serve as a crucial regulator underlying the phenotypic divergence in myofiber development between AA and TY chickens. In vitro experiments demonstrated that knockdown of DUSP1 significantly inhibited myogenic differentiation while overexpression of DUSP1 significantly promoted myogenic differentiation. Additionally, knockdown of DUSP1 enhanced p38 MAPK phosphorylation, promoted mitochondrial biogenesis and function, increased the oxidative metabolic capacity of myofibers, and stimulated the formation of type I muscle fibers. Conversely, overexpression of DUSP1 inhibited p38 MAPK phosphorylation and mitochondrial biogenesis and function, increased the anaerobic glycolytic capacity of myofibers, and promoted the transformation of muscle fibers from type I to type II. Blocking the p38 MAPK signaling pathway with SB203580 significantly inhibited the phenotypic changes caused by DUSP1 knockdown. In conclusion, the differential expression of the DUSP1 in the pectoral muscle of AA and TY chickens serves as a critical factor contributing to the disparity in myofiber development between the two breeds. It could promote myogenic differentiation and also regulate the transformation of muscle fiber types through the p38 MAPK/PGC-1α signaling pathway.