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Research Project: Validate Causative Mutations in Agriculturally-Important Vertebrates

Location: Plant Genetics Research

Title: Mitochondrial dysfunction is a hallmark of woody breast myopathy in broiler chickens

Author
item GREENE, ELIZABETH - University Of Arkansas
item Chen, Paula
item WALK, CARRIE - Ab Vista
item BEDFORD, MIKE - Ab Vista
item DRIDI, SAMI - University Of Arkansas

Submitted to: Frontiers in Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/27/2025
Publication Date: N/A
Citation: N/A

Interpretive Summary: Demand for poultry, specifically chicken meat, is projected to increase over the coming decades. Selection for faster growth and meat yield has been successful; however, there has been a rise in growth-related abnormalities that impact production, welfare, and sustainability. Specifically, woody breast is a muscle pathology that is characterized by hard nodules in the breast muscle that negatively impacts meat quality and is a significant welfare concern. Previous research has shown that development of woody breast is associated with restricted blood flow and decreased oxygen levels in the breast muscle. The present study was conducted to determine if mitochondria, which generate energy for the cell, are adversely affected during woody breast progression. In woody breast muscle, the mitochondria were swollen and had impaired function, which was due to excessive calcium accumulation and abnormal gene expression. These results unveiled previously unknown cellular mechanisms of woody breast progression that may be useful when determining methods of mitigating this pathology.

Technical Abstract: The woody breast (WB) myopathy poses significant economic and welfare concerns to the poultry industry; however, there is no effective strategy to mitigate this pathology due to its unknown etiology. After showing previously that hypoxia is a key factor in WB progression, we used various techniques demonstrating dysregulated mitochondria (morphology, biogenesis, tethering, function, and bioenergetics) in WB-affected muscles and in hypoxic myoblasts compared to healthy tissues and normoxic cells, respectively. The increased levels of calcium (Ca2+) in both WB-affected tissues and hypoxic myoblasts suggested that mitochondrial Ca2+ overload is likely a leading cause for mitochondrial dysfunction that merits further in-depth investigation. These findings are the first, to the best of our knowledge, to provide fundamental insights into the underlying molecular mechanisms of WB and open new vistas for understanding the interplay between calcium, mitochondrial (dys)function, and avian muscle health for subsequent development of effective preventative/corrective strategies.