CKIP-1 regulates mammalian and zebrafish myoblast fusion

Journal of Cell Science
Dominique BaasEvelyne Goillot

Abstract

Multinucleated muscle fibres arise by fusion of precursor cells called myoblasts. We previously showed that CKIP-1 ectopic expression in C2C12 myoblasts increased cell fusion. In this work, we report that CKIP-1 depletion drastically impairs C2C12 myoblast fusion in vitro and in vivo during zebrafish muscle development. Within developing fast-twich myotome, Ckip-1 localises at the periphery of fast precursor cells, closed to the plasma membrane. Unlike wild-type myoblasts that form spatially arrayed multinucleated fast myofibres, Ckip-1-deficient myoblasts show a drastic reduction in fusion capacity. A search for CKIP-1 binding partners identified the ARPC1 subunit of Arp2/3 actin nucleation complex essential for myoblast fusion. We demonstrate that CKIP-1, through binding to plasma membrane phosphoinositides via its PH domain, regulates cell morphology and lamellipodia formation by recruiting the Arp2/3 complex at the plasma membrane. These results establish CKIP-1 as a regulator of cortical actin that recruits the Arp2/3 complex at the plasma membrane essential for muscle precursor elongation and fusion.

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Citations

May 20, 2015·Current Opinion in Genetics & Development·Ji Hoon KimElizabeth H Chen
Jul 3, 2013·Mechanisms of Development·Harriet E Jackson, Philip W Ingham
Sep 11, 2014·Nature Reviews. Molecular Cell Biology·Marc EdwardsJohn A Cooper
Oct 24, 2019·Cellular and Molecular Life Sciences : CMLS·Bide ChenTizhong Shan
Aug 22, 2015·Development·Jessica WilliamsAaron N Johnson
Mar 14, 2020·Developmental Biology·Kimberly J HromowykSharon L Amacher

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