Myh6-MerCreMer Mouse

The Myh6 gene encodes the α-myosin heavy chain (α-MHC), a critical contractile protein predominantly expressed in cardiomyocytes, with species-specific variation in its spatial distribution: in humans, it is highly abundant in the atria and minimally expressed in adult ventricles (where β-MHC/MYH7 dominates), whereas in rodents, it serves as the primary ventricular motor protein ^[1]. This gene produces a "fast" myosin ATPase that drives rapid actin-myosin cross-bridge cycling, directly influencing cardiac contraction velocity, force generation, and power output. Myh6 expression dynamically regulates cardiac development and function; its downregulation (e.g., in heart failure or pressure overload) shifts the α-MHC/β-MHC ratio toward slower contraction, reducing cardiac efficiency and contributing to systolic dysfunction. Additionally, Myh6 hosts the intronic miRNA miR-208a, which fine-tunes stress-responsive gene networks, including thyroid hormone signaling and fetal gene reprogramming during hypertrophy ^[2]. Beyond contractile roles, Myh6 serves as a key marker for cardiomyocyte identity validation in cellular reprogramming and stem cell differentiation studies.

Myh6-MerCreMer mice were generated by inserting a Tamoxifen-inducible Cre recombinase protein MerCreMer gene expression element controlled by the mouse Myh6 promoter into the mouse H11 safe harbor site. Before induction, MerCreMer is only present in the cytoplasm and can only enter the nucleus to exert its recombination effect after Tamoxifen treatment. When bred with mice containing a loxP site-flanked sequence, Cre recombinase-mediated deletion of the flanked sequence will occur in the cardiomyocytes of the offspring after Tamoxifen induction. Compared with the Myh6-CreEsr1 mouse strain (Catalog No.: C001443), this strain shows improved survival outcomes in mice after tamoxifen induction.