PS1-10. Early Transcriptomic Signature of Hypoxia-induced Metabolic Shifts in Myositis and Wooden Breast.

Abstract Wooden Breast (WB) is a prevalent myopathy in modern commercial broilers characterized by palpable firmness and gross lesions of the Pectoralis (p.) major muscle. Histological evaluations have identified presence of myositis, along with phlebitis, myofiber degeneration, and foam cell accumulation in the affected tissue. Previous transcriptomic profiling of WB in adult broilers identified key genes linked with altered energy metabolism and hypoxia in the affected population. In this study, we performed transcriptome profiling of myositis in female broilers necropsied at post-hatch ages 14-17. Tissue samples of p. major muscle were evaluated using histopathological analyses to assess the presence or absence of myositis, followed by long-read RNA-seq on the Oxford Nanopore platform. A total of 14 samples were included, comprising 3 unaffected samples and 11 samples from birds with myositis-affected tissue. We identified 25 differentially expressed genes (FDR < 0.05; |logFC| > 1). PFKFB3 was the most significantly downregulated gene (-3.9 logFC), which is a key regulator of glycolysis and glucose uptake. Prior WB transcriptomic study has also reported PFKFB3 to be linked with disrupted glucose metabolism under hypoxic conditions in affected adult broilers. Downregulation of DGAT2 and PDK4 further indicated disrupted lipid and energy metabolism as a previous transcriptomic-metabolic study reported mitochondrial dysfunction and impaired glycerolipid metabolism. Upregulation of RRAD and SGK1 implicate glycolysis inhibition and cellular stress response, respectively. Enrichment analysis revealed oxygen and carbon dioxide transportation as the most significantly perturbed biological process. Notably, multiple genes encoding different hemoglobin subunits (HBBA, HBAD, HBA1, HBE1) were significantly downregulated in affected muscle. Taken together, the early-stage transcriptomic evidence of hypoxia and energy metabolism may mediate myofiber damage and inflammation resulting in myositis, although gross macroscopic lesions in the p. major muscle is not observed until 3 weeks of age.