Bertin, B. | bioRxiv Science

bioRxiv2019

A polarized nucleus-cytoskeleton-ECM connection controls collective migration and cardioblasts number in Drosophila

The formation of the cardiac tube is a remarkable example of complex morphogenetic process conserved from invertebrates to humans. It involves coordinated collective migration of contralateral rows of cardiac cells. The molecular processes underlying the specification of cardioblasts prior to migration are well established and significant advances have been made in understanding the process of lumen formation. However, the mechanisms of collective cardiac cells migration remain elusive. Here we identified CAP and MSP-300 as novel actors involved in cardioblast migration. They both display highly similar temporal and spatial expression pattern in migrating cardiac cells and are required for the correct number, alignment and coordinated directional migration of cardioblasts. Our data suggest that CAP and MSP-300 are part of a tension-sensitive protein complex linking cardioblast focal adhesion sites to nuclei via actin cytoskeleton and triggering coordinated cardioblast movements.

developmental biology↗

bioRxiv2019

New muscle identity code components identified by TRAP control shape and size of muscle subsets in Drosophila

A combinatorial code of identity transcription factors (iTFs) specifies the diversity of muscle types in Drosophila. We previously showed that two iTFs, Lms and Ap, play critical role in the identity of a subset of larval body wall muscles, the lateral transverse (LT) muscles. Intriguingly, a small portion of ap and lms mutants displays an increased number of LT muscles, a phenotype that recalls pathological split muscle fibers in human. However, genes acting downstream of Ap and Lms to prevent these aberrant muscle feature are not known. Here, we applied a cell type specific translational profiling (TRAP) to identify gene expression signatures underlying identity of muscle subsets including the LT muscles. We found that Gelsolin (Gel) and dCryAB, both encoding actin-interacting proteins, displayed LT muscle prevailing expression positively regulated by, the LT iTFs. Loss of dCryAB function resulted in LTs with irregular shape and occasional branched ends also observed in ap and lms mutant contexts. In contrast, enlarged and then split LTs with a greater number of myonuclei formed in Gel mutants while Gel gain of function resulted in unfused myoblasts, collectively indicating that Gel regulates LTs size and prevents splitting by limiting myoblast fusion. Thus, dCryAB and Gel act downstream of Lms and Ap and contribute to preventing LT muscle branching and splitting. Our findings offer first clues to still unknown mechanisms of pathological muscle splitting commonly detected in human dystrophic muscles and causing muscle weakness.

developmental biology↗