Myosin light chain kinase and Src control membrane dynamics in volume recovery from cell swelling

Barfod, Elisabeth T.; Moore, Ann L.; Graaf, Benjamin G. Van de; Lidofsky, Steven D.

doi:10.1091/mbc.e10-06-0514

Cited by 22 publications

(29 citation statements)

References 71 publications

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“…2 A) suggest that ROCK-mediated contractile force is mainly involved in the formation of polar blebs induced by local heating, but the contribution of MLCK-mediated force is limited. Y-27632 is known to inhibit osmotic stressinduced blebbing, but ML-7 does not suppress the blebbing (50). Our results are consistent with these observations.…”

Section: Discussionsupporting

confidence: 92%

Directional Bleb Formation in Spherical Cells under Temperature Gradient

Oyama

Arai

Isaka

et al. 2015

Biophysical Journal

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Living cells sense absolute temperature and temporal changes in temperature using biological thermosensors such as ion channels. Here, we reveal, to our knowledge, a novel mechanism of sensing spatial temperature gradients within single cells. Spherical mitotic cells form directional membrane extensions (polar blebs) under sharp temperature gradients (≥∼0.065°C μm(-1); 1.3°C temperature difference within a cell), which are created by local heating with a focused 1455-nm laser beam under an optical microscope. On the other hand, multiple nondirectional blebs are formed under gradual temperature gradients or uniform heating. During heating, the distribution of actomyosin complexes becomes inhomogeneous due to a break in the symmetry of its contractile force, highlighting the role of the actomyosin complex as a sensor of local temperature gradients.

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Section: Discussionsupporting

confidence: 92%

Directional Bleb Formation in Spherical Cells under Temperature Gradient

Oyama

Arai

Isaka

et al. 2015

Biophysical Journal

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“…We also found that phosphorylation of Tyr-158 does not affect the phosphorylation of the myosin regulatory light chain, 7 which is achieved by MLCK and is required for activation of myosin II motor activity (15). Interestingly, Src was previously shown recruited to membrane blebs where it associates with MLCK and myosin II (34,35). In response to cell swelling, Src and MLCK form a complex in which Src activates MLCK, and both regulate a compensatory membrane retrieval that requires myosin II (35).…”

Section: Discussionmentioning

confidence: 69%

“…Interestingly, Src was previously shown recruited to membrane blebs where it associates with MLCK and myosin II (34,35). In response to cell swelling, Src and MLCK form a complex in which Src activates MLCK, and both regulate a compensatory membrane retrieval that requires myosin II (35). It is thus conceivable that Src and MLCK could work together to fine-tune the activity of myosin II in the context of infection.…”

Section: Discussionmentioning

confidence: 99%

Src-dependent Tyrosine Phosphorylation of Non-muscle Myosin Heavy Chain-IIA Restricts Listeria monocytogenes Cellular Infection

Almeida

Mesquita

Cruz

et al. 2015

Journal of Biological Chemistry

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Background: Non-muscle myosin IIA is involved in force generation, movement, and membrane reshaping. Its activity is regulated by phosphorylation of the light chain. Results: NMHC-IIA head domain is tyrosine-phosphorylated by Src and modulates Listeria intracellular levels. Conclusion: Tyrosine phosphorylation of NMHC-IIA affects the outcome of infection. Significance: This novel post-translational modification of NMHC-IIA possibly affects its functions.

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“…10 Of note, Src was recently shown to complex with MLCK and affect its function. 6 Interestingly, upon PDGF stimulation, immunofluorescent staining indicates that MLCK colocalizes with CDRs (Fig. 7a).…”

Section: Resultsmentioning

confidence: 93%

Substrate Stiffness Regulates PDGF-Induced Circular Dorsal Ruffle Formation Through MLCK

et al. 2013

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As atherosclerosis progresses, vascular smooth muscle cells (VSMCs) invade from the medial layer into the intimal layer and proliferate, contributing to atherosclerotic plaque formation. This migration is stimulated in part by platelet-derived growth factor (PDGF), which is released by endothelial cells and inflammatory cells, and vessel stiffening, which occurs with age and atherosclerosis progression. PDGF induces the formation of circular dorsal ruffles (CDRs), actin-based structures associated with increased cell motility. Here we show that mechanical changes in matrix stiffness enhance the formation of CDRs in VSMCs in response to PDGF stimulation. Our data indicate that matrix stiffness increases cellular contractility, and that intracellular pre-stress is necessary for robust CDR formation. When treated with agonists that promote contractility, cells increase CDR formation, whereas agonists that inhibit contractility lead to decreased CDR formation. Substrate stiffness promotes CDR formation in response to PDGF by upregulating Src activity through myosin light chain kinase. Together, these data indicate that vessel stiffening accompanying atherogenesis may exacerbate VSMC response to PDGF leading to CDR formation.

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Myosin light chain kinase and Src control membrane dynamics in volume recovery from cell swelling

Abstract: MLCK resolves membrane blebbing induced by osmotic cell swelling. Cell swelling also stimulates the formation of a Src–MLCK complex, which with cortactin and dynamin forms actin-based structures at the base of the cell to facilitate membrane retrieval for volume recovery.

Cited by 22 publications

References 71 publications

Directional Bleb Formation in Spherical Cells under Temperature Gradient

Directional Bleb Formation in Spherical Cells under Temperature Gradient

Src-dependent Tyrosine Phosphorylation of Non-muscle Myosin Heavy Chain-IIA Restricts Listeria monocytogenes Cellular Infection

Substrate Stiffness Regulates PDGF-Induced Circular Dorsal Ruffle Formation Through MLCK

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