Key result
Wnt/β-catenin hyperactivation causes muscle hypertrophy and degeneration, rescued by Myostatin in zebrafish.
Why the study?
A tight regulation of Wnt/beta-catenin signaling is essential for muscle fiber growth and maintenance, but its role in slow and fast muscle myofibrillogenesis and interaction with Myostatin is not fully understood.
Hypothesis-generating in zebrafish; leaves open relevance to human muscle disorders without further validation.
Deviation from proper muscle development or homeostasis results in various myopathic conditions. Employing genetic as well as chemical intervention, we provide evidence that a tight regulation of Wnt/beta-catenin signaling is essential for muscle fiber growth and maintenance. In zebrafish embryos, gain-of-Wnt/beta-catenin function results in unscheduled muscle progenitor proliferation, leading to slow and fast muscle hypertrophy accompanied by fast muscle degeneration. The effects of Wnt/beta-catenin signaling on fast muscle hypertrophy were rescued by misexpression of Myostatin or p21(CIP/WAF), establishing an in vivo regulation of myofibrillogenesis by Wnt/beta-catenin signaling and Myostatin. Epistatic analyses suggest a possible genetic interaction between Wnt/beta-catenin and Myostatin in regulation of slow and fast twitch muscle myofibrillogenesis.
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Tee et al. (2009) studied Muscle development / Myofibrillogenesis. Wnt/β-catenin hyperactivation (genetic and chemical) vs. Wild-type embryos was evaluated on Muscle fiber growth and maintenance (hypertrophy and degeneration). Hyperactivation of Wnt/β-catenin signaling in zebrafish embryos causes unscheduled muscle progenitor proliferation, leading to muscle hypertrophy and degeneration that is rescued by Myostatin.
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