Myosin II isoforms identify distinct functional modules that support integrity of the epithelial zonula adherens

Smutny, Michael; Cox, Hayley L.; Leerberg, Joanne M.; Kovács, Éva; Conti, Mary Anne; Ferguson, Charles; Hamilton, Nicholas A.; Parton, Robert G.; Adelstein, Robert S.; Yap, Alpha S.

doi:10.1038/ncb2072

Cited by 302 publications

(394 citation statements)

References 37 publications

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“…20 We then examined the localization of non-muscle myosin II in MCF-7 cells depleted of Coronin 1B, as E-cadherin and F-actin have been shown to influence the recruitment of non-muscle myosin II to junctions. 4,6,19 As previously described, 4,6,19 NMIIA and NMIIB concentrated prominently at the zonulae adherente of control MCF-7 monolayers (Fig. 1D, E).…”

Section: Resultsmentioning

confidence: 84%

“…These structures are especially apparent in polarized epithelial cells, where prominent actomyosin bundles lie adjacent to the E-cadherin rings found at the apical region of cell-cell junctions, also known as the zonula adherens (ZA). [4][5][6] The physical coupling of actomyosin to E-cadherin adhesions results in contractile tension at junctions, which supports tissue cohesion, epithelial integrity and morphogenesis. [7][8][9][10][11][12][13] The assembly and activity of junctional actomyosin is subject to regulation by numerous cell signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 In epithelia, prominent contractile networks are found in the apical poles of embryonic epithelial cells (medioapical networks 3 ) and at the cortices of cell-cell adherens junctions (AJ). [4][5][6] At the AJs, actomyosin networks interact with E-cadherin-based adhesions that couple adjacent cells together to form cohesive monolayers. These structures are especially apparent in polarized epithelial cells, where prominent actomyosin bundles lie adjacent to the E-cadherin rings found at the apical region of cell-cell junctions, also known as the zonula adherens (ZA).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

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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.

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Section: Resultsmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

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“…Therefore, it is likely that non-muscle myosin IIA and B have two distinct functions, both in human and murine megakaryopoiesis. These two myosin II isoforms have previously been shown to have distinct roles in cadherin junction of the epithelial cells 31 or in the erythroblast enucleation 32 . However, MYH10 silencing does not explain the entire polyploidization process.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, abnormalities in the G1/S transition check point might also be present in the 4N MK 3,33,34 . In addition, it remains to understand why MYH9 does not accumulate in the cleavage furrow of MK in contrast to other cell types; in fact, myosin II isoform localization may depend on distinct upstream signalling pathways as shown in epithelial cells 31 .…”

Section: Discussionmentioning

confidence: 99%

RUNX1-induced silencing of non-muscle myosin heavy chain IIB contributes to megakaryocyte polyploidization

et al. 2012

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megakaryocytes are unique mammalian cells that undergo polyploidization (endomitosis) during differentiation, leading to an increase in cell size and protein production that precedes platelet production. Recent evidence demonstrates that endomitosis is a consequence of a late failure in cytokinesis associated with a contractile ring defect. Here we show that the non-muscle myosin IIB heavy chain (mYH10) is expressed in immature megakaryocytes and specifically localizes in the contractile ring. mYH10 downmodulation by short hairpin RnA increases polyploidization by inhibiting the return of 4n cells to 2n, but other regulators, such as of the G1/s transition, might regulate further polyploidization of the 4n cells. Conversely, re-expression of mYH10 in the megakaryocytes prevents polyploidization and the transition of 2n to 4n cells. During polyploidization, mYH10 expression is repressed by the major megakaryocyte transcription factor RunX1. Thus, RunX1-mediated silencing of mYH10 is required for the switch from mitosis to endomitosis, linking polyploidization with megakaryocyte differentiation.

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Cell Adhesion Structures in Epithelial Cells Are Formed in Dynamic and Cooperative Ways

Shigetomi

Ikenouchi

2019

BioEssays

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There are many morphologically distinct membrane structures with different functions at the surface of epithelial cells. Among these, adherens junctions (AJ) and tight junctions (TJ) are responsible for the mechanical linkage of epithelial cells and epithelial barrier function, respectively. In the process of new cell-cell adhesion formation between two epithelial cells, such as after wounding, AJ form first and then TJ form on the apical side of AJ. This process is very complicated because AJ formation triggers drastic changes in the organization of actin cytoskeleton, the activity of Rho family of small GTPases, and the lipid composition of the plasma membrane, all of which are required for subsequent TJ formation. In this review, the authors focus on the relationship between AJ and TJ as a representative example of specialization of plasma membrane regions and introduce recent findings on how AJ formation promotes the subsequent formation of TJ. Figure 6. Addition of cholesterol restores the formation of TJ in α-catenin KO cells. Time-lapse imaging of α-catenin KO epithelial cells expressing GFP-claudin-3. Cholesterol-saturated MβCD (75 mM) was added to the medium to restore the level of cholesterol in the plasma membrane at time 0. GFP-claudin-3 gradually accumulate at the cell-cell interface and TJ is formed even in the absence of AJ. Scale bar, 20 µm. Adapted with permission. [72]

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Myosin II isoforms identify distinct functional modules that support integrity of the epithelial zonula adherens

Cited by 302 publications

References 37 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

RUNX1-induced silencing of non-muscle myosin heavy chain IIB contributes to megakaryocyte polyploidization

Cell Adhesion Structures in Epithelial Cells Are Formed in Dynamic and Cooperative Ways

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