Research groups

Gene regulation and morphogenesis

Dr Beatriz Estrada. UPO
Myogenesis, a model system to study tissue development
Dr Beatriz Estrada. UPO
Researcher associated to Dr Maria Dolores (Lola) Martín Bermudo. CSIC

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We are investigating the development and maintenance of Drosophila musculature as a model system to better understand tissue formation and homeostasis. Muscle development is a multistep process that is conserved across the animal kingdom. It requires several cellular processes such as myoblast fusion, muscle guidance and attachment to the tendons, and final differentiation of the myofibrils. We are studying the genetic and molecular mechanisms underlying these processes through genetic analyses, in vivo visualization of myogenesis and molecular characterization of protein interactions. One of the genes we are studying is perdido, (perd, also known as Kon-tiki), encoding a conserved cell adhesion proteoglycan, which is essential for the formation of proper muscle projections and stable attachments to the tendon cells. We are investigating the molecules that mediate how muscles recognize their tendons and establish stable attachment sites. Muscle differentiation requires the assembly of higher-order structures called myofibrils, composed of sarcomeres. Even though the molecular organization of sarcomeres is well known, the mechanisms underlying myofibrillogenesis are poorly understood. Integrin-dependent adhesion is required to initiate the assembly of myofibrils both in vertebrates and in Drosophila. We have observed that Perd is essential for the nucleation of myofibrils to sustain sarcomere assembly in adult muscles. In comparison to controls, perd-depleted muscles contain fewer myofibrils, localized at the cell periphery. These myofibrils are detached from each other and display a defective sarcomeric structure. We suggest that Perd acts downstream or in parallel to integrins to enable the connection of nascent myofibrils to the Z-bands. We are analyzing the downstream signaling pathways that regulate myofibrillogenesis. Interestingly, there are several human myopathies related to failure in these cellular processes. These findings may help in diagnosing and ultimately treating some muscular diseases.