Rho GTPase and Shroom direct planar polarized actomyosin contractility during convergent extension

Simões, Sérgio; Mainieri, Avantika; Zallen, Jennifer A.

doi:10.1083/jcb.201307070

Cited by 131 publications

(133 citation statements)

References 52 publications

Supporting

Mentioning

123

Contrasting

Unclassified

Order By: Relevance

“…7 RhoA signaling is a master regulator of actomyosin cytoskeleton and thus has been implicated in a variety of morphogenetic processes. [31][32][33][34][35][36] While the role for active RhoA signaling in facilitating essential cellular processes has been wellestablished 9,[37][38][39][40][41] there are circumstances where RhoA signaling must be downregulated, either physiologically or pathologically to elicit a biological response. 41,42 Given the importance of the actomyosin cytoskeleton in positively regulating RhoA signaling, 7,[43][44][45] targeting actin-regulators such as Coronin 1B might be one of the approaches to achieve a precise spatiotemporal regulation of RhoA.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2016

View full text Add to dashboard Cite

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.

show abstract

Section: Resultsmentioning

confidence: 99%

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

et al. 2016

View full text Add to dashboard Cite

show abstract

“…S9A), respectively. Together, these Simões et al, 2014;Warrington et al, 2013). In the C. elegans dorsal epidermis, by contrast, zygotic rho-1(ok2418) mutants or epidermal-specific RHO-1(T17N) embryos can still intercalate, even though cytokinesis has failed and the cells are binucleate in the latter (E.W.-S. and J.H., unpublished).…”

Section: Discussionmentioning

confidence: 99%

Polarized Rac-dependent protrusions drive epithelial intercalation in the embryonic epidermis of C. elegans

2015

View full text Add to dashboard Cite

Cell intercalation is a fundamental, coordinated cell rearrangement process that shapes tissues throughout animal development. Studies of intercalation within epithelia have focused almost exclusively on the localized constriction of specific apical junctions. Another widely deployed yet poorly understood alternative mechanism of epithelial intercalation relies on basolateral protrusive activity. Using the dorsal embryonic epidermis of C. elegans, we have investigated this alternative mechanism using high-resolution live cell microscopy and genetic analysis. We find that as dorsal epidermal cells migrate past one another, they produce F-actin rich protrusions polarized at their extending (medial) edges. These protrusions are controlled by the C. elegans Rac and RhoG orthologs, CED-10 and MIG-2, which function redundantly to polarize actin polymerization upstream of the WAVE complex and WASP, respectively. We also identify UNC-73, the C. elegans ortholog of Trio, as a guanine nucleotide exchange factor (GEF) upstream of both CED-10/Rac and MIG-2/RhoG. Further, we identify a novel polarizing cue, CRML-1, the ortholog of human Capping Arp2/3 Myosin I Linker (CARMIL), that localizes to the nonprotrusive lateral edges of dorsal cells. CRML-1 genetically suppresses UNC-73/Trio function, and indirectly, actin polymerization. This network identifies a novel, molecularly conserved cassette that regulates epithelial intercalation via basolateral protrusive activity.

show abstract

“…Elongation is reduced in embryos deficient for myosin-II heavy chain, myosin regulatory light chain (MRLC), Rok, which activates MRLC, or Shroom (Bertet et al, 2004;Simões et al, 2010Simões et al, , 2014. Furthermore, disruption of Par-3, Par-6 or aPKC also impairs elongation (Blankenship et al, 2006;Simões et al, 2010;Zallen and Wieschaus, 2004), potentially due to roles for these proteins in rosette formation.…”

Section: Drosophila Epithelial Morphogenesismentioning

confidence: 98%

“…Intercalating cells in the epithelium initially establish planar polarity, which is first identifiable by the asymmetric enrichment of F-actin at the AP borders between cells (Blankenship et al, 2006). Myosin-II and its activator Rho kinase (Rok, a homolog of Rock) also accumulate at AP borders and promote localized junctional contraction (Bertet et al, 2004;Zallen and Wieschaus, 2004;Simões et al, 2010) and, recently, the scaffolding protein Shroom was shown to be required for Rok and myosin-II junctional activation, downstream of Rok signaling (Simões et al, 2014). Subsequently, AJs, as assayed by staining for β-catenin (Armadillo) and E-cadherin (Shotgun), become enriched (Haas and Gilmour, 2006; modified with permission from Harding and Nechiporuk, 2012).…”

Section: Drosophila Epithelial Morphogenesismentioning

confidence: 99%

The roles and regulation of multicellular rosette structures during morphogenesis

2014

View full text Add to dashboard Cite

Multicellular rosettes have recently been appreciated as important cellular intermediates that are observed during the formation of diverse organ systems. These rosettes are polarized, transient epithelial structures that sometimes recapitulate the form of the adult organ. Rosette formation has been studied in various developmental contexts, such as in the zebrafish lateral line primordium, the vertebrate pancreas, the Drosophila epithelium and retina, as well as in the adult neural stem cell niche. These studies have revealed that the cytoskeletal rearrangements responsible for rosette formation appear to be conserved. By contrast, the extracellular cues that trigger these rearrangements in vivo are less well understood and are more diverse. Here, we review recent studies of the genetic regulation and cellular transitions involved in rosette formation. We discuss and compare specific models for rosette formation and highlight outstanding questions in the field.

show abstract

Rho GTPase and Shroom direct planar polarized actomyosin contractility during convergent extension

Abstract: Rho GTPase signaling establishes a planar polarized actomyosin network within which the actin-binding protein Shroom enhances myosin activity locally to generate robust mechanical forces during axis elongation.

Cited by 131 publications

References 52 publications

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

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

Polarized Rac-dependent protrusions drive epithelial intercalation in the embryonic epidermis of C. elegans

The roles and regulation of multicellular rosette structures during morphogenesis

Contact Info

Product

Resources

About