Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II

Cell Cycle. 2016 Nov 16;15(22):3033-3041. doi: 10.1080/15384101.2016.1234549. Epub 2016 Sep 20.

Abstract

Non-muscle myosin II (NMII) motor proteins are responsible for generating contractile forces inside eukaryotic cells. There is also a growing interest in the capacity for these motor proteins to influence cell signaling through scaffolding, especially in the context of RhoA GTPase signaling. We previously showed that NMIIA accumulation and stability within specific regions of the cell cortex, such as the zonula adherens (ZA), allows the formation of a stable RhoA signaling zone. Now we demonstrate a key role for Coronin 1B in maintaining this junctional pool of NMIIA, as depletion of Coronin 1B significantly compromised myosin accumulation and stability at junctions. The loss of junctional NMIIA, upon Coronin 1B knockdown, perturbed RhoA signaling due to enhanced junctional recruitment of the RhoA antagonist, p190B Rho GAP. This effect was blocked by the expression of phosphomimetic MRLC-DD, thus reinforcing the central role of NMII in regulating RhoA signaling.

Keywords: Coronin 1B; Feedback; NMIIA; RhoA; p190B.

MeSH terms

  • 4-Butyrolactone / analogs & derivatives*
  • 4-Butyrolactone / metabolism
  • Actomyosin / metabolism
  • Adherens Junctions / metabolism
  • Caco-2 Cells
  • Cadherins / metabolism
  • Epithelial Cells / metabolism
  • GTPase-Activating Proteins / metabolism
  • Guanosine Triphosphate / metabolism
  • Humans
  • Intercellular Junctions / metabolism*
  • MCF-7 Cells
  • Models, Biological
  • Myosin Light Chains / metabolism
  • Nonmuscle Myosin Type IIA / metabolism*
  • Phenotype
  • Protein Stability
  • Signal Transduction*
  • rhoA GTP-Binding Protein / metabolism*

Substances

  • Cadherins
  • GTPase-Activating Proteins
  • Myosin Light Chains
  • coronin
  • Guanosine Triphosphate
  • Actomyosin
  • Nonmuscle Myosin Type IIA
  • rhoA GTP-Binding Protein
  • 4-Butyrolactone