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

Abstract

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.

Cardiac ECM: Its Epigenetic Regulation and Role in Heart Development and Repair

“…In the middle development, the mechanism of dorsal closure could also be a sophisticated method, involving associate degree orchestration of cell-matrix interaction between smooth muscle cells, epithelial tissue cells, and the ECM [20]. A recent study demonstrated that nucleus-cytoskeleton-ECM connections triggered coordinated cardioblast movements, and controlled cardioblast number in Drosophila [21]. In this review, we will focus on the role of the ECM in the regulation of cardiac development and repair.…”

“…Sci. 2020, 21, 8610 2 of 20 collagens, laminin, elastin, fibulins, proteoglycans, matrix metalloproteinases (MMPs), tenascin-C (TNC), and thrombospodins (TSPs) [18]. In addition, immune cells in the cardiac microenvironment can also produce ECM proteins such as MMPs to modulate the immune response in the heart, contributing to the regulation of cardiomyocyte survival [19].…”