Myh7 Conditional Knockout mouse models

Beta myosin heavy chain is encoded by Myh7, ortholog of human MYH7, a slow ATPase motor whose head domain hydrolyzes ATP to drive actin filament sliding and whose rod mediates thick filament assembly, including the folded interacting heads motif that sets the super-relaxed state and therefore baseline energy consumption. Species context governs interpretation, since beta myosin dominates the human ventricle while the adult mouse ventricle runs mainly on alpha myosin from Myh6, so a mouse null is comparatively uninformative and reinduction of Myh7 is read as a marker of the fetal gene program in stress. Human missense variants cause hypertrophic and dilated cardiomyopathy through altered super-relaxed state occupancy, which is precisely the target of mavacamten, making patient-specific knockins or humanized alleles the correct instruments rather than deletion. Match alleles to endpoints including echocardiographic wall thickness, myofibrillar ATPase and loaded shortening, single-molecule motility, and myocardial disarray on histology.

Tissue restricted knockout of Myh7 keeps wild type function everywhere else. Breeding is often more robust, and the setup mirrors patient biology where mutations arise in a subset of cells.