Molecular genetic and epigenetic mechanisms of regulation of meat productivity in chickens: recent findings on epigenetic, metabolic and breed features

The contemporary poultry production industry is confronted with the imperative to enhance meat productivity, a goal that necessitates a comprehensive grasp of the molecular, genetic, and epigenetic mechanisms governing growth regulation. This review analyzes current data on molecular genetic and epigenetic mechanisms regulating meat production in chickens. The study places particular emphasis on key genes (GHR, MSTN, GNPDA2, LDB2, KPNA3), exploring their roles in muscle tissue development, metabolism, and the influence of environmental factors. The results of transcriptomic studies demonstrating differences in gene expression between commercial broilers and local breeds, as well as the role of epigenetic modifications in adaptation to stressful conditions and nutrition, are summarized. The present study demonstrates that selection for accelerated growth is associated with the activation of anabolic pathways (IGF-1, PI3K/Akt), yet concomitantly increases the risk of developing muscular myopathies. As shown, the expression profiles observed in the pectoral and leg muscles, as well as in the hypothalamus, indicate the tissue-specific nature of growth regulation. The review emphasizes the necessity of considering genetic diversity and epigenetic plasticity in breeding programs and the potential of multi-omics approaches to enhance the efficiency of poultry production. The data reviewed here provide a basis for developing innovative strategies to optimize growth, meat quality, and bird adaptation to changing environmental conditions. Such strategies may include an in-depth study of gene interactions, the development of marker-assisted breeding programs, and the application of nutriepigenomics. This paper examines the molecular genetic and epigenetic mechanisms regulating meat productivity in chickens, focusing on current data concerning epigenetic, metabolic, and breed-specific factors.