Dynamic myosin activation promotes collective morphology and migration by locally balancing oppositional forces from surrounding tissue.
Migrating cells need to overcome physical constraints from the local microenvironment to navigate their way through tissues. Cells that move collectively have the additional challenge of negotiating complex environments in vivo while maintaining cohesion of the group as a whole. The mechanisms by which collectives maintain a migratory morphology while resisting physical constraints from the surrounding tissue are poorly understood. Drosophila border cells represent a genetic model of collective migration within a cell-dense tissue. Border cells move as a cohesive group of 6-10 cells, traversing a network of large germ line-derived nurse cells within the ovary. Here we show that the border cell cluster is compact and round throughout their entire migration, a shape that is maintained despite the mechanical pressure imposed by the surrounding nurse cells. Nonmuscle myosin II (Myo-II) activity at the cluster periphery becomes elevated in response to increased constriction by nurse cells. Furthermore, the distinctive border cell collective morphology requires highly dynamic and localized enrichment of Myo-II. Thus, activated Myo-II promotes cortical tension at the outer edge of the migrating border cell cluster to resist compressive forces from nurse cells. We propose that dynamic actomyosin tension at the periphery of collectives facilitates their movement through restrictive tissues.
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195 Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH 44106.
George
G
Aranjuez
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.
Ashley
A
Burtscher
Division of Biology, Kansas State University, Manhattan, KS 66506.
Ketki
K
Sawant
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195 pralay.dbs@presiuniv.ac.in jmcdona@ksu.edu.
Pralay
P
Majumder
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195 Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH 44106 Division of Biology, Kansas State University, Manhattan, KS 66506 pralay.dbs@presiuniv.ac.in jmcdona@ksu.edu.
Jocelyn A
JA
McDonald
D008841:Actin Cytoskeleton / Q000378:metabolism; D000205:Actomyosin / Q000378:metabolism; D000818:Animals; D002465:Cell Movement / Q000502:physiology; D048430:Cell Shape / Q000502:physiology; D060833:Cellular Microenvironment; D004330:Drosophila / Q000235:genetics / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D005260:Female; D024462:Myosin Type II / Q000378:metabolism*; D009218:Myosins / Q000502:physiology*; D009866:Oogenesis; D015398:Signal Transduction / Q000235:genetics
D029721:Drosophila Proteins; D000205:Actomyosin; D024462:Myosin Type II; D009218:Myosins