Isoform B of myosin II heavy chain mediates actomyosin contractility during TNFα-induced apoptosis

Solinet, Sara; Vitale, María Leiza

doi:10.1242/jcs.022640

Cited by 16 publications

(17 citation statements)

References 57 publications

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“…Finally, the death of a cell also involves contractility that affects several aspects of cell death at both the structural and molecular levels, such as release of nuclear RanGTP, compaction and entosis (Moss et al, 2009;Overholtzer et al, 2007;Smadja-Lamere et al, 2008;Solinet and Vitale, 2008).…”

Section: Cellular Functions Of the Contractomementioning

confidence: 99%

The contractome – a systems view of actomyosin contractility in non-muscle cells

Zaidel-Bar

Guo

Luxenburg

2015

Journal of Cell Science

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Actomyosin contractility is a highly regulated process that affects many fundamental biological processes in each and every cell in our body. In this Cell Science at a Glance article and the accompanying poster, we mined the literature and databases to map the contractome of non-muscle cells. Actomyosin contractility is involved in at least 49 distinct cellular functions that range from providing cell architecture to signal transduction and nuclear activity. Containing over 100 scaffolding and regulatory proteins, the contractome forms a highly complex network with more than 230 direct interactions between its components, 86 of them involving phosphorylation. Mapping these interactions, we identify the key regulatory pathways involved in the assembly of actomyosin structures and in activating myosin to produce contractile forces within non-muscle cells at the exact time and place necessary for cellular function.

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Section: Cellular Functions Of the Contractomementioning

confidence: 99%

The contractome – a systems view of actomyosin contractility in non-muscle cells

Zaidel-Bar

Guo

Luxenburg

2015

Journal of Cell Science

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“…Communal et al (43) have reported that β-adrenergic stimulation via norepinephrine exposure in adult rat ventricular cardiomyocytes triggered a caspase 3 targeting of α-actin, α-actinin, and cardiac troponin T before the onset of apoptosis. More recently, other sarcomeric proteins have been shown to be direct caspase targets in apoptotic models including, myosin heavy chain and ventricular myosin light chain (44)(45)(46). The ability of caspase 3 to directly modify cellular structure while altering the activity of key gene expression programs implies that this protease (and the intrinsic pathway) may serve as a fulcrum for agonistinduced hypertrophy in general.…”

Section: Activation Of the Intrinsic Cell Death Pathway Is Required Formentioning

confidence: 99%

Intrinsic-mediated caspase activation is essential for cardiomyocyte hypertrophy

Putinski

Abdul‐Ghani

Stiles

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Cardiomyocyte hypertrophy is the cellular response that mediates pathologic enlargement of the heart. This maladaptation is also characterized by cell behaviors that are typically associated with apoptosis, including cytoskeletal reorganization and disassembly, altered nuclear morphology, and enhanced protein synthesis/ translation. Here, we investigated the requirement of apoptotic caspase pathways in mediating cardiomyocyte hypertrophy. Cardiomyocytes treated with hypertrophy agonists displayed rapid and transient activation of the intrinsic-mediated cell death pathway, characterized by elevated levels of caspase 9, followed by caspase 3 protease activity. Disruption of the intrinsic cell death pathway at multiple junctures led to a significant inhibition of cardiomyocyte hypertrophy during agonist stimulation, with a corresponding reduction in the expression of known hypertrophic markers (atrial natriuretic peptide) and transcription factor activity [myocyte enhancer factor-2, nuclear factor kappa B (NF-κB)]. Similarly, in vivo attenuation of caspase activity via adenoviral expression of the biologic effector caspase inhibitor p35 blunted cardiomyocyte hypertrophy in response to agonist stimulation. Treatment of cardiomyocytes with procaspase 3 activating compound 1, a small-molecule activator of caspase 3, resulted in a robust induction of the hypertrophy response in the absence of any agonist stimulation. These results suggest that caspase-dependent signaling is necessary and sufficient to promote cardiomyocyte hypertrophy. These results also confirm that cell death signal pathways behave as active remodeling agents in cardiomyocytes, independent of inducing an apoptosis response.

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“…The specificity of these antibodies has been shown elsewhere (Solinet and Vitale 2008). Mouse monoclonal anti-cortactin (clone 4F11), polyclonal anti-Par3 and goat polyclonal anti-vimentin were from Chemicon (Temecula, CA, USA).…”

Section: Source Of Antibodies and Chemicalsmentioning

confidence: 99%

“…Pre-cleared supernatants (2 mg protein/ml) were incubated with either buffer (control) or with the immunoprecipitating antibody overnight at 4°C on an orbital rocker. One hundred microlitre of protein A Sepharose 4B beads, pre-washed with PBS, were added to each sample and the mixtures were further incubated for 4 h at 4°C (Solinet and Vitale 2008). Beads were rinsed several times in lysis buffer, and were finally resuspended in 30 ll electrophoresis sample buffer and boiled for 5 min.…”

Section: Coimmunoprecipitation Studiesmentioning

confidence: 99%

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Myosin IIB deficiency in embryonic fibroblasts affects regulators and core members of the par polarity complex

Solinet

Akpovi

Garcia

et al. 2011

Histochem Cell Biol

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Wild-type (WT) and myosin heavy chain IIB null [MHCIIB (-/-)] embryonic fibroblasts were used as an experimental model to assess the role of the isoform B of myosin II (MII) in the regulation of the cell shape and intrinsic polarity. Genetic ablation of MHCIIB causes a persistent albeit, unstable protrusive activity in embryonic fibroblasts (Lo et al. in Nonmuscle myosin IIB is involved in the guidance of fibroblast migration. Mol Biol Cell 15:982-989, 2004). Here, we show that MHCIIB-deficient fibroblasts are characterized by a sustained guanine nucleotide exchange factor (GEF)-dependent activation of the small GTPase Rac-1 that is responsible for the continual lamellipodium formation. Moreover, we observed a sustained PKC-ζ activation and an increased association of cortactin with the plasma membrane in the MHCIIB (-/-) cells that were also dependent on GEF-mediated Rac-1 activation. Rac-1 activation and its downstream effects were induced in WT fibroblasts by inhibiting MII ATPase and crosslinking activities, suggesting that an altered actin-MII interaction favours Rac-1 activation, regardless of the MII isoform implicated. In addition, we found MIIB isoform-specific effects that were independent of Rac-1 activation. MHCIIA interacts with cortactin whereas MHCIIB does not. By contrast, MHCIIB interacts with Lgl1, a member of the Scribble/Dlg/Lgl polarity complex, whereas MHCIIA does not. MHCIIB (-/-) fibroblasts exhibited deregulated endogenous levels of the Par polarity complex members, Par3 and Par6. Together, the data show that MHCIIB deficiency causes imbalances in signalling pathways that are responsible for cell polarity determination. The results suggest that these pathways are targets of MIIB in the regulation of the cell's shape and polarity.

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Isoform B of myosin II heavy chain mediates actomyosin contractility during TNFα-induced apoptosis

Cited by 16 publications

References 57 publications

The contractome – a systems view of actomyosin contractility in non-muscle cells

The contractome – a systems view of actomyosin contractility in non-muscle cells

Intrinsic-mediated caspase activation is essential for cardiomyocyte hypertrophy

Myosin IIB deficiency in embryonic fibroblasts affects regulators and core members of the par polarity complex

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