RT Journal Article SR Electronic T1 Regionalized tissue fluidization by an actomyosin cable is required for epithelial gap closure during insect gastrulation JF bioRxiv FD Cold Spring Harbor Laboratory SP 744193 DO 10.1101/744193 A1 A. Jain A1 V. Ulman A1 A. Mukherjee A1 M. Prakash A1 L. Pimpale A1 S. Muenster A1 K.A. Panfilio A1 F. Jug A1 S.W. Grill A1 P. Tomancak A1 A. Pavlopoulos YR 2019 UL http://biorxiv.org/content/early/2019/08/22/744193.1.abstract AB Many animal embryos face early on in development the problem of having to pull and close an epithelial sheet around the spherical yolk-sac. During this gastrulation process, known as epiboly, the spherical geometry of the egg dictates that the epithelial sheet first expands and subsequently compacts to close around the sphere. While it is well recognized that contractile actomyosin cables can drive epiboly movements, it is unclear how pulling on the leading edge can lead to simultaneous tissue expansion and compaction. Moreover, the epithelial sheet spreading over the sphere is mechanically stressed and this stress needs to be dissipated for seamless closure. While oriented cell division is known to dissipate tissue stresses during epiboly in zebrafish, it is unclear how this is achieved in organisms that do not exhibit cell divisions during epiboly. Here we show that during extraembryonic tissue (serosa) epiboly in the red flour beetle Tribolium castaneum, the non-proliferative serosa becomes regionalized into two distinct territories: a dorsal region under higher tension away from the leading edge with larger, isodiametric and non-rearranging cells, and a more fluid ventral region under lower tension surrounding the leading edge with smaller, anisotropic cells undergoing cell intercalation. Our results suggest that fluidization of the leading edge is caused by a heterogeneous actomyosin cable that drives sequential eviction and intercalation of individual cells away from the serosa margin. Since this developmental solution utilized during epiboly resembles the mechanism of wound healing in other systems, we propose actomyosin cable-driven local tissue fluidization as a conserved morphogenetic module for closure of epithelial gaps.