Cytoplasmic Protrusions in Insect Cells During Mitosis in Vitro

Tokumitsu, Takashi; Maramorosch, Karl

doi:10.1083/jcb.34.2.677

Cited by 17 publications

(6 citation statements)

References 12 publications

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“…Blebbing of the plasma membrane is quite a common cellular process accompanying cytokinesis (32), migration (33), virus uptake (34), and apoptosis (35). In addition, cytoplasmic blebbing of the plasma membrane has been observed during physical and chemical stress and usually is preceded by an elevation of intracellular Ca 2ϩ that has to rise Ͼ ϳ300 nM concentration (36).…”

Section: Discussionmentioning

confidence: 99%

Cell-penetrating Peptides Split into Two Groups Based on Modulation of Intracellular Calcium Concentration

Lorents

Kodavali

Oskolkov

et al. 2012

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Cell-penetrating Peptides Split into Two Groups Based on Modulation of Intracellular Calcium Concentration

Lorents

Kodavali

Oskolkov

et al. 2012

Journal of Biological Chemistry

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“…More recently, research has re-focused on non-apoptotic blebs that are characterized by their smaller size and more uniform morphology than those of apoptotic cells. Such PM blebs are observed during physiologically distinct processes such as cytokinesis, amoeboid types of invasive motility, and cell adhesion [17][18][19]. Blebbing can also be induced experimentally, e.g.…”

Section: Introductionmentioning

confidence: 99%

Differing and isoform-specific roles for the formin DIAPH3 in plasma membrane blebbing and filopodia formation

et al. 2011

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Plasma membrane (PM) blebs are dynamic actin-rich cell protrusions that occur, e.g., during cytokinesis, amoeboid cell motility and cell attachment. Using a targeted siRNA screen against 21 actin nucleation factors, we identify a novel and essential role of the human diaphanous formin DIAPH3 in PM blebbing during cell adhesion. Suppression of DIAPH3 inhibited blebbing to promote rapid cell spreading involving β1-integrin. Multiple isoforms of DIAPH3 were detected on the mRNA and protein level of which isoforms 3 and 7 were the largest and most abundant isoforms that however did not induce formation of actin-rich protrusions. Rather, PM blebbing specifically involved the low abundance isoform 1 of DIAPH3 and activation of isoform 7 by deletion of the diaphanous-autoregulatory domain caused the formation of filopodia. Dimerization and actin assembly activity were essential for induction of specific cell protrusions by DIAPH3 isoforms 1 and 7. Our data suggest that the N-terminal region comprising the GTPasebinding domain determined the subcellular localization of the formin as well as its protrusion activity between blebs and filopodia. We propose that isoform-selective actin assembly by DIAPH3 exerts specific and differentially regulated functions during cell adhesion and motility.

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“…Blebs are spherical membrane protrusions that commonly occur at the cortex during cytokinesis, cell spreading, virus uptake, and apoptosis (3)(4)(5)(6)(7). Moreover, increasing evidence points to an essential role for blebs as leading edge protrusions during cell migration in three-dimensional environments, particularly during embryonic development and tumor-cell dissemination (8-11; reviewed in refs.…”

mentioning

confidence: 99%

Role of cortical tension in bleb growth

Tinévez

Schulze

Salbreux³

et al. 2009

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

502

575

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Blebs are spherical membrane protrusions often observed during cell migration, cell spreading, cytokinesis, and apoptosis, both in cultured cells and in vivo. Bleb expansion is thought to be driven by the contractile actomyosin cortex, which generates hydrostatic pressure in the cytoplasm and can thus drive herniations of the plasma membrane. However, the role of cortical tension in bleb formation has not been directly tested, and despite the importance of blebbing, little is known about the mechanisms of bleb growth. In order to explore the link between cortical tension and bleb expansion, we induced bleb formation on cells with different tensions. Blebs were nucleated in a controlled manner by laser ablation of the cortex, mimicking endogenous bleb nucleation. Cortical tension was modified by treatments affecting the level of myosin activity or proteins regulating actin turnover. We show that there is a critical tension below which blebs cannot expand. Above this threshold, the maximal size of a bleb strongly depends on tension, and this dependence can be fitted with a model of the cortex as an active elastic material. Together, our observations and model allow us to relate bleb shape parameters to the underlying cellular mechanics and provide insights as to how bleb formation can be biochemically regulated during cell motility.T he cell cortex is a thin meshwork of actin filaments, myosin, and associated proteins that lies beneath the plasma membrane (1). Because of the presence of active myosin motors, which slide filaments with respect to one another in the network, the cortex is under tension. As a result, the cortex exerts pressure on the cytoplasm and can actively contract, driving cell deformations (2).Blebs are spherical membrane protrusions that commonly occur at the cortex during cytokinesis, cell spreading, virus uptake, and apoptosis (3-7). Moreover, increasing evidence points to an essential role for blebs as leading edge protrusions during cell migration in three-dimensional environments, particularly during embryonic development and tumor-cell dissemination (8-11; reviewed in refs. 7, 12). Despite the importance of blebbing, very little is known about the mechanisms of bleb growth.The life cycle of a bleb can be subdivided into three phases (7, 13). First, a bleb is nucleated, either by local detachment of the cortex from the plasma membrane or by local rupture of the cortex. In the subsequent growth phase, a membrane bulge, initially devoid of cortex, expands from the nucleation site. Finally, the cortex gradually reassembles at the bleb membrane, leading to bleb retraction.Bleb formation is often correlated with high myosin II activity, and myosin II inhibition prevents blebbing (6,7,10,14). For that reason, and because of their round shape and rapid expansion, blebs are commonly believed to be a direct mechanical consequence of the hydrostatic pressure exerted on the cytoplasm by the contractile cortex, which would drive bleb growth from places of local cortex weakening without any further r...

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Cytoplasmic Protrusions in Insect Cells During Mitosis in Vitro

Cited by 17 publications

References 12 publications

Cell-penetrating Peptides Split into Two Groups Based on Modulation of Intracellular Calcium Concentration

Cell-penetrating Peptides Split into Two Groups Based on Modulation of Intracellular Calcium Concentration

Differing and isoform-specific roles for the formin DIAPH3 in plasma membrane blebbing and filopodia formation

Role of cortical tension in bleb growth

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