PUBLICATION
Arl13b and the non-muscle myosin heavy chain IIA are required for circular dorsal ruffle formation and cell migration
- Authors
- Casalou, C., Seixas, C., Portelinha, A., Pintado, P., Barros, M., Ramalho, J.S., Lopes, S.S., Barral, D.C.
- ID
- ZDB-PUB-140513-66
- Date
- 2014
- Source
- Journal of Cell Science 127(Pt 12): 2709-22 (Journal)
- Registered Authors
- Lopes, Susana
- Keywords
- ARL13B, Myosin heavy chain IIA, Myh9, Circular dorsal ruffle, Small G protein, Actin cytoskeleton, Platelet-derived growth factor signaling, Wound healing
- MeSH Terms
-
- ADP-Ribosylation Factors/metabolism*
- Animals
- Cell Movement*
- Cell Surface Extensions/metabolism*
- Endosomes/metabolism
- HeLa Cells
- Humans
- Mice
- NIH 3T3 Cells
- Nonmuscle Myosin Type IIA/metabolism*
- Pinocytosis
- Protein Transport
- Zebrafish
- PubMed
- 24777479 Full text @ J. Cell Sci.
Citation
Casalou, C., Seixas, C., Portelinha, A., Pintado, P., Barros, M., Ramalho, J.S., Lopes, S.S., Barral, D.C. (2014) Arl13b and the non-muscle myosin heavy chain IIA are required for circular dorsal ruffle formation and cell migration. Journal of Cell Science. 127(Pt 12):2709-22.
Abstract
The Arf-like protein Arl13b has been implicated in ciliogenesis and Sonic hedgehog signaling. Furthermore, we have previously shown that it regulates endocytic recycling traffic and interacts with actin. Herein, we report that the non-muscle myosin heavy chain IIA, also known as Myh9, is an Arl13b effector. Moreover, we found that both proteins localize to circular dorsal ruffles (CDRs) induced by platelet-derived growth factor stimulation and are required for their formation. CDRs are ring-shaped actin-dependent structures formed on the dorsal cell surface and have been involved in diverse processes such as macropinocytosis, integrin recycling, internalization of receptor tyrosine kinases and cell migration. We found that Arl13b or Myh9 silencing impairs cell migration, suggesting that Arl13b is required for this function through the interaction with Myh9. Moreover, Arl13b silencing impairs neural crest cell migration in zebrafish embryos. Furthermore, we show that Arl13b is required for the formation of CDRs in migrating cells. Thus, our results indicate a novel role for Arl13b in actin cytoskeleton remodeling through the interaction with Myh9, by driving the formation of CDRs necessary for cell migration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping