Open AccessDrosophila Activin signaling promotes muscle growth through InR/dTORC1 dependent and independent processes
Author(s) -
Myung Joon Kim,
Michael B. O’Connor
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.190868
Subject(s) - biology , myostatin , acvr2b , activin type 2 receptors , myosin , medicine , signal transduction , activin receptor , endocrinology , microbiology and biotechnology , skeletal muscle , transforming growth factor , tgf beta signaling pathway
The Myostatin/Activin branch of the TGFβ superfamily acts as a negative regulator of vertebrate skeletal muscle size, in part, through downregulation of insulin/IGF-1 signaling. Surprisingly, recent studies in Drosophila indicate that motoneuron derived Activin signaling acts as a positive regulator of muscle size. Here we demonstrate that Drosophila Activin signaling promotes growth of the muscle cells along all three axes; width, thickness and length. Activin signaling positively regulates the InR/dTORC1 pathway and the level of Mhc, an essential sarcomeric protein, via increased Pdk1 and Akt1 expression. Enhancing InR/dTORC1 signaling in the muscle of Activin pathway mutants restores Mhc levels close to wild-type, but only increases muscle width. In contrast, hyperactivation of the Activin pathway in muscles increases overall larval body and muscle fiber length even when Mhc levels were lowered by suppression of dTORC1. Together, these results indicate that the Drosophila Activin pathway regulates larval muscle geometry and body size via promoting InR/dTORC1-dependent Mhc production and the differential assembly of sarcomeric components into either pre-existing or new sarcomeric units depending on the balance of InR/dTORC1 and Activin signals.