Emerging roles of MICAL family proteins – from actin oxidation to membrane trafficking during cytokinesis
Open Access
- 1 January 2017
- journal article
- research article
- Published by The Company of Biologists in Journal of Cell Science
- Vol. 130 (9), 1509-1517
- https://doi.org/10.1242/jcs.202028
Abstract
Cytokinetic abscission is the terminal step of cell division, leading to the physical separation of the two daughter cells. The exact mechanism mediating the final scission of the intercellular bridge connecting the dividing cells is not fully understood, but requires the local constriction of endosomal sorting complex required for transport (ESCRT)-III-dependent helices, as well as remodelling of lipids and the cytoskeleton at the site of abscission. In particular, microtubules and actin filaments must be locally disassembled for successful abscission. However, the mechanism that actively removes actin during abscission is poorly understood. In this Commentary, we will focus on the latest findings regarding the emerging role of the MICAL family of oxidoreductases in F-actin disassembly and describe how Rab GTPases regulate their enzymatic activity. We will also discuss the recently reported role of MICAL1 in controlling F-actin clearance in the ESCRT-III-mediated step of cytokinetic abscission. In addition, we will highlight how two other members of the MICAL family (MICAL3 and MICAL-L1) contribute to cytokinesis by regulating membrane trafficking. Taken together, these findings establish the MICAL family as a key regulator of actin cytoskeleton dynamics and membrane trafficking during cell division.Keywords
Funding Information
- Institut Pasteur
- Centre National de la Recherche Scientifique
- Fondation pour la Recherche Médicale (DEQ20120323707)
- Institut National Du Cancer (2014-1-PL BIO-04-IP1)
- Agence Nationale de la Recherche (ANR-10-IDEX-0001-02 PSL)
- iXCore Foundation
- ANR Cytosign
- ANR AbCyStem
This publication has 99 references indexed in Scilit:
- EHD3 Protein Is Required for Tubular Recycling Endosome Stabilization, and an Asparagine-Glutamic Acid Residue Pair within Its Eps15 Homology (EH) Domain Dictates Its Selective Binding to NPF PeptidesPublished by Elsevier BV ,2016
- Modulation of MICAL Monooxygenase Activity by its Calponin Homology Domain: Structural and Mechanistic InsightsScientific Reports, 2016
- The Ciliopathy Protein CC2D2A Associates with NINL and Functions in RAB8-MICAL3-Regulated Vesicle TraffickingPLoS Genetics, 2015
- Phosphoinositides: Lipids with informative heads and mastermind functions in cell divisionBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, 2015
- Semaphorin3a Promotes Advanced Diabetic NephropathyDiabetes, 2014
- GRAF1 forms a complex with MICAL-L1 and EHD1 to cooperate in tubular recycling endosome vesiculationFrontiers in Cell and Developmental Biology, 2014
- MICAL-like1 mediates epidermal growth factor receptor endocytosisMolecular Biology of the Cell, 2011
- Boundary cap cells constrain spinal motor neuron somal migration at motor exit points by a semaphorin-plexin mechanismNeural Development, 2007
- Drosophila MICAL regulates myofilament organization and synaptic structureMechanisms of Development, 2007
- Expression of Novel Molecules, MICAL2-PV (MICAL2 Prostate Cancer Variants), Increases with High Gleason Score and Prostate Cancer ProgressionClinical Cancer Research, 2006