Key result
Cardiomyocyte-specific overexpression of a short isoform of α-adducin and its phospho-mimic variants, along with γ-adducin, induced persistent sarcomere disassembly in adult mice.
Why the study?
Cardiomyocyte mitosis remains poorly understood, including how sarcomeres are disassembled during mitosis to allow abscission of daughter cardiomyocytes.
Does adducin overexpression induce sarcomere disassembly in mammalian cardiomyocytes?
Does adducin overexpression induce sarcomere disassembly in mammalian cardiomyocytes?
Adducin regulates sarcomere disassembly during cardiomyocyte mitosis, providing mechanistic insights into cytoskeletal morphological changes relevant to cardiomyopathy.
Hypothesis-generating for adducin in cardiomyopathy cytoskeletal pathology; requires validation in human models.
Recent interest in understanding cardiomyocyte cell-cycle has been driven by potential therapeutic applications in cardiomyopathy. However, despite recent advances, cardiomyocyte mitosis remains a poorly understood process. For example, it is unclear how sarcomeres are disassembled during mitosis to allow abscission of daughter cardiomyocytes. Here we identify adducin as a regulator of sarcomere disassembly during mammalian cardiomyocyte mitosis. α/γ-adducins are selectively expressed in neonatal mitotic cardiomyocytes, and their levels decline precipitously thereafter. Cardiomyocyte-specific overexpression of various splice isoforms and phosphoforms of α-adducin in-vitro and in-vivo identified Thr445/Thr480 phosphorylation of a short isoform of α adducin as a potent inducer of neonatal cardiomyocyte sarcomere disassembly. Concomitant overexpression of this α-adducin variant along with γ-adducin resulted in stabilization of the adducin complex and persistent sarcomere disassembly in adult mice, which is mediated by interaction with α-actinin. These results highlight an important mechanism for coordination of cytoskeletal morphological changes during cardiomyocyte mitosis.
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Xiao et al. (2020) studied Cardiomyocyte mitosis and regeneration. Adducin overexpression (Add1 i2, phospho-mimic T445E/T480E, Add3) vs. Wild-type or control vector was evaluated on Sarcomere disassembly in cardiomyocytes. Cardiomyocyte-specific overexpression of a short isoform of α-adducin and its phospho-mimic variants, along with γ-adducin, induced persistent sarcomere disassembly in adult mice.
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