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Research in the Henry Lab

We wish to understand the role and influence of key players in muscle formation and in the development of muscular dystrophy, aiming to develop treatments or therapies that can support damaged and diseased tissue at the molecular level.

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A large variety of diseases, both inherited and acquired, affect muscle tissues in humans. In order to prevent and treat such diseases, it is necessary to understand their pathology at the cellular and molecular level. Because each step of muscle specification and differentiation translates to a progressive refinement of functional physiology, studying muscle development may lead to therapeutic insights. The goal of our laboratory is to elucidate the signaling networks that underlie muscle morphogenesis, specifically with respect to muscular dystrophy.

Although many of the genes that contribute to muscular dystrophy are known, the fundamental cell biology of attachment is not yet understood. Treatments for muscular dystrophy will require both gene identification and an intricate understanding of how gene products function in their cellular network.

To achieve this end, we study skeletal muscle morphogenesis during zebrafish development. Skeletal muscle is comprised of segmentally reiterated myotomes. Like the mammalian tendon, the zebrafish myotome boundary transduces force from muscle to the skeletal system. Thus, myotome boundary formation, as well as skeletal muscle morphogenesis, is critical for normal development and muscle function. By focusing on genes that are important in the myotome boundary we can observe their role in cell adhesion and identify treatments for muscular dystrophies caused by those genes.

The zebrafish is an excellent model system with which to integrate the genetic, molecular, and cell biological mechanisms that underlie muscle development. In zebrafish, like in mice, homologues of the dystoglycan complex are conserved and disruption in members of this complex, such as laminin, dystroglycan, or dystropin, the gene implicated in Duchenne muscular dystrophy, also cause muscular dystrophy-like failures of muscle cells to differentiate or maintain attachment to the extracellular matrix. Because the signaling networks that regulate muscle development are so remarkably conserved among vertebrates, our studies may lead to novel insights into development of therapeutics for muscle and tendon diseases.

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