An hspb1-null mouse to depict the contribution of hsp27 in beef tenderness
Résumé
In order to examine the role of Hsp27 in the molecular mechanisms of Beef tenderness, we generated an HspB1-null mouse. The mutant mouse was viable, fertile and showed neither apparent morphological nor anatomical alterations. The macroscopic or microscopic muscle phenotype was not altered. However, there were evidences for a muscle-type specific alteration of the molecular phenotype in relation to 1) apoptosis, Hsp status and anti-oxidant status in an oxidative muscle and 2) Hsp status and calcium homeostasis in a glycolytic muscle. Lastly, electron microscopy revealed ultrastructural abnormalities in the myofibrillar structure of mutant mice. These data suggest that Hsp27 could directly impact the organization of muscle cytoskeleton and contribute to tenderness at the molecular and ultrastructural levels.