ライフサイエンスコーパス: myosin II

1 gulator, NUAK2, or by inhibition of Rho-ROCK-myosin II.

2 as previously discovered to inhibit skeletal myosin II.

3 c cancer cells by binding to non-muscle (NM) myosin II.

4 traction of the resultant actin filaments by myosin II.

5 intercalation within the cochlea all require myosin II.

6 pressure generation by delocalizing cortical myosin II.

7 ion of a complex between RhoA, S100A4 and NM myosin II.

8 phenotypes are surprisingly both mediated by myosin II.

9 l ring rich in actin filaments and nonmuscle myosin II.

10 ity to phosphorylate and activate non-muscle myosin II.

11 r Lgl1 disrupts the cellular localization of myosin II.

12 arity of migrating cells by Scrib, Lgl1, and myosin II.

13 tein actin and the molecular motor nonmuscle myosin II.

14 mechanism at about the velocity of load-free myosin II.

15 nts, the Rho effectors diaphanous formin and myosin-II.

16 folds, formin, and the tail of the essential myosin-II.

17 tion and become contractile and sensitive to myosin-II.

18 ulates the mono-ubiquitination of non-muscle Myosin II, a protein associated with hearing loss in hum

19 ROCK-myosin II ablation specifically kills resistant cells vi

20 hanges in retraction at the cell rear, while myosin II accumulation at the rear exhibits a reproducib

21 We identified that increased nonmuscle myosin II activation and cellular contraction inhibited

22 asia, spectrin mutant cells, despite showing myosin II activation and Yki-mediated hyperplasia, parad

23 e exchange factor ECT-2, is upstream of both myosin-II activation and diaphanous formin-mediated fila

24 y arrayed actomyosin fibers are resilient to myosin-II activation.

25 The myosin II activator Rho-kinase (Rok) is planar polarized

26 independent of its established function as a myosin II activator, but requires a microtubule-dependen

27 Our results show that myosin II activity and actin polymerization increase cor

28 ealed that amoeboid melanoma cells with high Myosin II activity are predominant in the invasive front

29 High ROCK-myosin II activity correlates with aggressiveness, ident

30 Similarly, higher Myosin II activity enhances the integrin multilayering p

31 Moreover, loss of myosin II activity has opposing effects on protrusive ac

32 Proteomic analysis shows that ROCK-Myosin II activity in amoeboid cancer cells controls an

33 an array of tumor models, we show that high Myosin II activity in tumor cells reprograms the innate

34 We report that myosin II activity is regulated by PKC during 5-HT respo

35 By reducing myosin II activity or knocking down alpha-actinin, we fo

36 Interestingly, myosin II activity stiffens the cortex and branched acti

37 rapy response, drug-resistant clones restore myosin II activity to increase survival.

38 dimensional (2D) substrate rigidity promotes myosin II activity to increase traction force in a proce

39 MAPK regulates myosin II activity, but after initial therapy response,

40 We show here that high Myosin II activity, high levels of ki-67 and high tumour

41 This strictly depended on myosin II activity, suggesting local network reorganizat

42 usions where F-actin is devoid of non-muscle myosin II activity.

43 tes were also dependent on Rac1, formin, and myosin II activity.

44 retrograde actin network flow and nonmuscle myosin II activity.

45 S depletion was previously shown to decrease myosin II activity.

46 ed by down-regulation of RHOA expression and myosin II activity.

47 nduced by perturbations that alter nonmuscle myosin II activity.

48 or CIE of MHCI and CD59 through promotion of myosin II activity.

49 nase (ROCK) controlled excessive contractile myosin-II activity and not to elevated F-actin polymeriz

50 RhoA-mediated regulation of myosin-II activity in the actin cortex controls the abil

51 Although actin polymerization or myosin-II activity individually enhances fluctuations, t

52 Furthermore, we show that Myosin-II activity is a significant driver of this trans

53 ucleus across many matrices, timescales, and myosin-II activity levels indicates a constant ratio of

54 The main cause is a cytoplasmic increase in myosin-II activity that could sterically hinder chromoso

55 NM myosin II actomyosin cross-bridge cycling regulates the

56 By activating myosin II along Ne/Epi junctions ahead of the zipper and

57 junctions ahead of the zipper and inhibiting myosin II along newly formed Ne/Ne junctions behind the

58 Here, we show that non-muscle myosin II, alpha-actinin, and filamin accumulate to mech

59 While actin and myosin II also play critical roles in the formation of r

60 Loss of myosin II also selectively inhibits myofibroblast differ

61 le in cell division among protists that lack myosin II and additionally implicate the broad use of me

62 All three phenomena depend on myosin II and are temporally correlated with the pulses

63 binds to the heavy chain of non-muscle (NM) myosin II and can regulate the motility of crawling cell

64 epithelium, which displays planar-polarized myosin II and experiences anisotropic forces from neighb

65 Both myosin II and phosphoinositide 3-kinase (PI3K) were foun

66 that WNT11-FZD7-DAAM1 activates Rho-ROCK1/2-Myosin II and plays a crucial role in regulating tumour-

67 br3 mutants phenocopy pathogenic variants of Myosin II and that Ubr3 interacts genetically and physic

68 uclear stiffness resulting from increases in myosin-II and lamin-A,C.

69 formation of podosomes by inhibition of RhoA/myosin-II and promotion of actin core assembly.

70 actomyosin ring (AMR), composed of F-actin, myosin II, and other actin and myosin II regulators.

71 Scrib also forms a complex with myosin II, and Scrib, Lgl1, and myosin II colocalize at

72 ded by the SVIL gene, is a large sarcolemmal myosin II- and F-actin-binding protein.

73 align the Fn matrix by increasing nonmuscle myosin II- and platelet-derived growth factor receptor a

74 In muscle cells, actin filaments and myosin II appear in a polarized structure called a sarco

75 INTS: Non-muscle (NM) and smooth muscle (SM) myosin II are both expressed in smooth muscle tissues, h

76 increase in diameter when actin filaments or myosin II are disrupted.

77 Myosin IIs are key players in the cell's ability to reac

78 This work defines novel roles for myosin II as a key regulatory effector molecule of the p

79 an optimum established by the percentage of myosin II assembled into bipolar filaments.

80 data demonstrate that multiple inputs to the myosin II assembly state integrate at the level of myosi

81 tion in airway SM by regulating a pool of NM myosin II at the cell cortex.

82 found no change in the levels of f-actin or myosin-II at the division plane when CYK-4 GAP activity

83 l tension is more sensitive to inhibition of myosin II ATPase activity than to inhibition of ROCK act

84 , and these are likely to underlie how other myosin II-based contractile systems are assembled.

85 ne point contacts is to restrain or "clutch" myosin-II-based filamentous actin (F-actin) retrograde f

86 In motile non-neuronal cells, myosin-II binds and exerts force upon actin filaments at

87 We show that initial Myosin II bipolar cell polarization gives way to unipola

88 These MTs suppress Rho activation, nonmuscle myosin II bipolar filament assembly, and actin retrograd

89 ends on the correct regulation of non-muscle Myosin II, but how this motor protein is spatiotemporall

90 hondrial constriction sites, whereas dynamic myosin II clouds are present in the vicinity of constric

91 r a ring of cross-linked actin filaments and myosin-II clusters, we derive the force balance equation

92 complex with myosin II, and Scrib, Lgl1, and myosin II colocalize at the leading edge of migrating ce

93 ation ability, also spontaneously generating myosin II concentration gradients in the solution phase

94 ion, whereas activation of Rho enhances acto-myosin II contractility and cell retraction.

95 ue of Science, Shyer et al. (2017) show that myosin II contractility drives the smooth dermal mesench

96 spatial organization of protrusion relies on myosin II contractility, and feedback between adhesion a

97 surfaces, and acts synergistically with RhoA/myosin-II contractility to further augment blebbing in c

98 that confinement-induced activation of RhoA/myosin-II contractility, coupled with LINC complex-depen

99 ts, junctional N-cadherin bonds downregulate Myosin-II contractility.

100 n under different force modes and inhibiting myosin II decreases cell stiffness, chromatin deformatio

101 In vivo, thorough depletion of nonmuscle myosin II delayed furrow initiation, slowed F-actin alig

102 ivate TGF-beta through a mechanism involving myosin II dependent contractility.

103 Survival of resistant cells is myosin II dependent, regardless of the therapy.

104 Our work suggests Cdh2 coordinates Myosin-II dependent internalisation of the zebrafish neu

105 on compliant 3D ECMs, and these effects are myosin-II dependent.

106 l junctions to keep them shut and to prevent myosin II-dependent contractility from tearing cadherin

107 , diffusion-based accumulation and a slower, myosin II-dependent cortical flow phase that acts on pro

108 and traction independently, suggesting these myosin II-dependent forces are generated by distinct mec

109 lls using RNA interference (RNAi) results in myosin II-dependent unzipping of cadherin adhesive bonds

110 ntal data and analytical modelling show that myosin-II-dependent force anisotropy within the lateral

111 d regulation of MT growth dynamics through a myosin-II-dependent signaling pathway.

112 Drp1 loss also leads to myosin II depletion at the membrane furrow, thereby resu

113 Abrogation of Cdh2 results in defective Myosin-II distribution, mislocalised internalisation eve

114 y excessive local cell proliferation, but by myosin II-driven cell contractility.

115 cer cells perpetuate their behavior via ROCK-Myosin II-driven IL-1alpha secretion and NF-kappaB activ

116 ROCK-Myosin II drives fast rounded-amoeboid migration in canc

117 ds to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue.

118 We describe an unexpected role for Myosin II dynamics in cancer cells controlling myeloid f

119 tingly, blocking activity of NMII (nonmuscle myosin II) either before, or after, lumen morphogenesis

120 t myosin: the D melanogaster skeletal muscle myosin II embryonic isoform (EMB).

121 In turning cells, myosin II exhibits dynamic side-to-side relocalization a

122 Myosin II exists as different isoforms that are involved

123 bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and pulling

124 have shown that inhibiting one of these-the myosin II family of cytoskeletal motors-blocks glioblast

125 We quantify myosin II filament dwell times and processivity as funct

126 he acto-myosin network and follow individual myosin II filament dynamics.

127 force is produced through sliding of bipolar myosin II filaments along actin filaments.

128 to both increasing dwell times of individual myosin II filaments and a global change from a remodelin

129 sin bundles involves registered alignment of myosin II filaments and their subsequent fusion into lar

130 Contractile arrays of actin and myosin II filaments drive many essential processes in no

131 gest that the CR may be derived from foci of myosin II filaments in a manner similar to what has been

132 In contrast, myosin II filaments in earlier stages of cytokinesis wer

133 copy indicated that within the CR, actin and myosin II filaments were organized into tightly packed l

134 concatenation and persistent association of myosin II filaments with each other and thus led to seve

135 Bud4 exclusively at the outer zones and with myosin-II filaments in the middle zone.

136 suggest an atomic model for the off state of myosin II, for its activation and unfolding by phosphory

137 unction disruption, redistribution of active myosin II from junctions to stress fibers, reduced tensi

138 ation of Rab35 compartments does not require Myosin II function.

139 However, it remains unclear whether these myosin II-generated cellular forces are produced simulta

140 vity of phosphatase PP1 to generate cortical myosin II gradients.

141 While nonmuscle myosin II has been studied extensively in the context of

142 myosin II tails to the plasma membrane, with myosin II heads extending into the cytoplasm.

143 n affects the upper 50 kDa sub-domain of the myosin II heavy chain, and cells carrying this lethal mu

144 Although, the non-muscle myosin II holoenzyme (myosin) is a molecular motor that

145 as up-regulated, 5-HT treatments resulted in myosin II hyperactivation accompanied by catastrophic co

146 stimulated the interaction of S100A4 with NM myosin II in airway SM at the cell cortex and catalysed

147 While activation of myosin II in Drosophila melanogaster pupal retina leads

148 A and IIB are the most prevalent isoforms of myosin II in glioblastoma, and we now show that codeleti

149 ine the structural organization of actin and myosin II in isolated cortical cytoskeletons prepared fr

150 the localization, dynamics, and functions of myosin II in migrating border cells of the Drosophila ov

151 ular function of non-muscle (NM) isoforms of myosin II in smooth muscle (SM) tissues and their possib

152 creased RhoA activity, anillin and nonmuscle myosin II in the cytokinetic ring, and faster cytokineti

153 ovel, to our knowledge, structural model for myosin-II in complex with actin and MgADP and compare ou

154 ogy in vivo using optogenetic stimulation of myosin-II in Drosophila embryos.

155 s, and the lamellipodium buckles upward in a myosin II-independent manner.

156 Nonmuscle myosin II inhibition (NMIIi) in the basolateral amygdala

157 Myosin II inhibition rescues rupture and DNA damage, imp

158 Here, myosin II inhibition rescues rupture and partially rescu

159 and they respond independently to actin and myosin II inhibition, serum deprivation and microtubule

160 However, when tension is reduced through myosin II inhibition, WT cells relax 3x faster to the fl

161 in response to matrix elasticity, knockdown, myosin-II inhibition, and even constricted migration tha

162 and contractions, but this can be blocked by myosin-II inhibition.

163 activity of fast skeletal and cardiac muscle myosin II, inhibition of skeletal muscle contractility e

164 results were mimicked by treatment with the myosin II inhibitor blebbistatin.

165 ons that resisted disassembly induced by the myosin II inhibitor, blebbistatin.

166 p to visualize the effect of blebbistatin, a myosin II inhibitor, on the morphodynamics of contractio

167 Myosin II is a key component of the actomyosin ring, alt

168 Non-muscle myosin II is found adjacent to mitochondria but is not s

169 rized structure called a sarcomere, in which myosin II is localized in the center.

170 clude that the assembly and activation of NM myosin II is regulated during contractile stimulation of

171 The role of myosin II is supported by the observation of an increase

172 Myosin II is the main force-generating motor during musc

173 Myosin II is the motor protein that enables muscle cells

174 formation and the concomitant inhibition of Myosin-II is required to induce invasion downstream of R

175 A hallmark feature of myosin-II is that it can spontaneously self-assemble int

176 ells depend on the late cytokinetic S. pombe myosin II isoform, Myp2p, a non-essential protein that i

177 immature megakaryocytes express 2 nonmuscle myosin II isoforms (MYH9 [NMIIA] and MYH10 [NMIIB]), onl

178 Here, we investigated the role of non-muscle myosin II isoforms (NMIIA and NMIIB) in epithelial junct

179 internalized by ROCK2-mediated activation of myosin II isoforms to mediate spatial regulation of CIE,

180 tinct myosin population containing nonmuscle myosin II isoforms, which is regulated by phosphorylatio

181 sphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.

182 mbly via the formin FMNL2 and Arp2/3, active myosin-II localization, and integrin-based adhesion dyna

183 for Dictyostelium myosin II, we predict that myosin II mechanoresponsiveness will be biphasic with an

184 rophils is impaired because of a decrease in myosin II-mediated contractility.

185 ere attenuated by blebbistatin inhibition of myosin II-mediated cytoskeletal contraction.

186 the myosin phosphatase, ERK and RSK promote myosin II-mediated tension for lamella expansion and opt

187 r envelope remnants soon after NEBD, and its myosin-II-mediated contraction reduces CSV and facilitat

188 ted regulation of MT growth persistence from myosin-II-mediated regulation of growth persistence spec

189 branching and shape change largely through a myosin-II-mediated reorganization of the actin and micro

190 h two distinct mechanisms: destabilizing the myosin II (MII) hexameric complex and inhibiting MII con

191 ize to anisotropic features under non-muscle myosin II (MII) inhibition, despite MII ordinarily being

192 dorsal root ganglion neurons, we found that myosin II (MII) is required for NGF to stimulate faster

193 actin, cross-linking proteins, and nonmuscle myosin II (MII), begins to reassemble on the membrane.

194 Our simulations also show how myosin II mini-filaments, in tandem with cross-linkers,

195 eshold value, inducing contraction driven by myosin II mini-filaments.

196 glycol and blocked ATP-powered compaction by myosin-II miniature filaments.

197 and the expression of myosin light chain of myosin II (MLC2), which was identified as another target

198 The organization of filamentous actin and myosin II molecular motor contractility is known to modi

199 egulation of Rho-kinase-dependent non-muscle myosin II motor activity.

200 ate that disease-associated mutations in the myosin II motor domain disrupt specific aspects of myosi

201 Cyclic interactions between myosin II motor domains and actin filaments that are pow

202 Myosin-18B co-localized with myosin II motor domains in stress fibers and was enriche

203 ed Rho-associated protein kinase-induced and myosin II motor inhibitor-induced barrier loss by limiti

204 The nonmuscle myosin II motor protein produces forces that are essenti

205 ipates in Rho-associated protein kinase- and myosin II motor-dependent (but not myosin light chain ki

206 e-sensitive cytoskeletal proteins, including myosin II motors and actin cross-linkers such as alpha-a

207 Actin cytoskeletal elements, including myosin II motors and actin crosslinkers, structurally re

208 stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.

209 Cells with inhibited myosin II motors increased traction force (from 41 nN to

210 Remarkably, beads coated with heavy-mero-myosin II motors showed a similar behavior.

211 ng shear stress and inhibition of non-muscle myosin II motors, respectively.

212 nt proteins, principally actin filaments and myosin-II motors.

213 pombe, we found that myo2-S1 (myo2-G515D), a Myosin II mutant allele, was capable of rescuing lethali

214 g area in cellularization similar to that in myosin II mutants.

215 Nonmuscle myosin II (Myo-II) activity at the cluster periphery bec

216 atase Pp1 complex, which inhibits non-muscle myosin-II (Myo-II) activity, coordinates border cell sha

217 isoforms have distinct roles: "Conventional myosin-II Myo2 is crucial to ring assembly, unconvention

218 we report two modes of control over Rho1 and myosin II (MyoII) activation in the Drosophila endoderm.

219 odelling requires the activity of non-muscle myosin II (MyoII) in the interphasic cells neighbouring

220 works are thought to contract when nonmuscle myosin II (myosin) is activated throughout a mixed-polar

221 is crucial to ring assembly, unconventional myosin-II Myp2 is most important for ring constriction,

222 formation has been correlated with nonmuscle myosin II (NM-II) activity.

223 Nonmuscle myosin II (NM-II) is an important motor protein involved

224 However, the mechanisms by which nonmuscle myosin II (NM-II) is recruited to those structures and a

225 ns of polymerized unphosphorylated nonmuscle myosin IIs (NM2s), and this is reversed by phosphorylati

226 We find that actin and non-muscle myosin II (NMII) assemble into previously undescribed po

227 Active non-muscle myosin II (NMII) enables migratory cell polarization and

228 Inhibition of non-muscle myosin II (NMII) enhances central but impairs peripheral

229 or by inhibiting the actin driver nonmuscle myosin II (NMII) in the BLA or systemically.

230 es the critical role of ezrin and non-muscle myosin II (NMII) in the progressive implementation of li

231 Non-muscle myosin II (NMII) is a conserved force-producing cytoskel

232 Nonmuscle myosin II (NMII) is uniquely responsible for cell contra

233 ll shape changes are controlled by nonmuscle myosin II (NMII) motor proteins, which are tightly regul

234 A nonmuscle myosin II (NMII) reporter revealed pulsatile contraction

235 To identify novel regulators of nonmuscle myosin II (NMII) we performed an image-based RNA interfe

236 Non-muscle myosin II (NMII)-induced multicellular contractility is

237 generated by the molecular motor, non-muscle myosin II (NMII).

238 alyzed the localization of axonal non-muscle myosin II (NMII).

239 We show that two isoforms of nonmuscle myosin II, NMIIA and NMIIB, control distinct steps of th

240 ion of both canonical anillin and non-muscle myosin II (NMM-II) to intercellular bridges.

241 d unbroken continuous rings, while nonmuscle myosin II (NMMII) formed linear tracts along the actin r

242 contractile actomyosin networks is nonmuscle myosin II (NMMII), a molecular motor that assembles into

243 s promotes the accumulation of the nonmuscle myosin II NMY-2 and the midbody component CYK-7 at the b

244 tile forces generated within it by nonmuscle myosin II (NMY-2) drive cellular morphogenetic processes

245 we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions.

246 hree of the five eukaryotic supergroups lack myosin II of the actomyosin contractile ring.

247 esting that they are selective for nonmuscle myosin II over skeletal myosin.

248 Multiple myosin II paralogues accumulate at mammalian epithelial

249 d changes in expression and activity of ROCK-myosin II pathway during acquisition of resistance to MA

250 easing and reducing the activity of the Rho1-Myosin II pathway enhances and decreases multilayering o

251 ed lumenization, disruption of ROCK-mediated myosin II phosphorylation, and SRC signaling, which led

252 ary-specific gene expression is regulated by myosin II phosphorylation, which increases actomyosin co

253 changes are accompanied by reorganization of Myosin II, PIP3, adhesion and active Cdc42.

254 equires active cell rearrangements driven by Myosin II planar polarisation.

255 NM myosin II plays a critical role in airway SM contraction

256 e an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based

257 downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions.

258 in RNA or small interfering RNA prevented NM myosin II polymerization as well as the recruitment of v

259 lts indicate that the two spatially distinct myosin II populations coordinately regulate ovulatory co

260 H9-related disease mutations into Drosophila myosin II produces motors with altered organization and

261 The mono-ubiquitination of Myosin II promotes its physical interaction with Myosin

262 We propose that myosin II promotes mitochondrial constriction by inducin

263 the actin cytoskeleton is reorganized, with myosin II recruited to the cortex, which may pressurize

264 tic impact of platelets, including nonmuscle myosin II, red blood cells (RBCs), fibrin(ogen), factor

265 monstrate that distinct and dynamic pools of myosin II regulate protrusion dynamics within and betwee

266 helial cells through aPKC activity-dependent myosin II regulation.

267 d of F-actin, myosin II, and other actin and myosin II regulators.

268 around the wound, and constitutively active myosin II regulatory light chain suppresses the effects

269 ities are associated with altered Rho-kinase/myosin II signaling and loss of apically distributed act

270 over, we identified a role for the RhoA-ROCK-myosin II signaling axis in this MeV internalization pro

271 vigation, was modestly dependent on Rho-ROCK-myosin II signaling on a 2D substrate or in a loose coll

272 lts reveal a critical role for myosin-18B in myosin II stack assembly and provide evidence that myosi

273 wever, mechanisms underlying the assembly of myosin II stacks and their physiological functions have

274 II stack assembly and provide evidence that myosin II stacks are important for a variety of vital pr

275 tress fibers and was enriched at the ends of myosin II stacks.

276 nd thus led to severely impaired assembly of myosin II stacks.

277 p1 on available rigor and blebbistatin-bound myosin II structures suggests that myo2-E1-Sup1 may repr

278 he base of the node that anchors the ends of myosin II tails to the plasma membrane, with myosin II h

279 Mutations in myosin II that are associated with human diseases are pr

280 synergistic relationship between cofilin and myosin II that is spatiotemporally regulated in the grow

281 are periodic pulses of junctional and medial myosin II that result in progressively stronger cortical

282 lthough velocity gradients were steeper with myosin II, the much larger bead diffusion observed with

283 ction is facilitated by actin and non-muscle myosin II through a mechanism that remains unclear, larg

284 ow that inputs that influence the ability of myosin II to assemble into filaments impact the ability

285 II assembly state integrate at the level of myosin II to govern the cellular response to mechanical

286 osin through the Rho-mediated recruitment of myosin II to the apical cortex.

287 ants failed to properly polarize and recruit myosin II to the cell rear essential for migration.

288 s generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhe

289 at the front of a cell, and PTEN to localize myosin II to the rear of a cell.

290 midzone MTs), whereas F-actin and non-muscle myosin II, together with other factors, organize into th

291 NM myosin II undergoes polymerization in airway SM and regu

292 of elongate, antiparallel filaments, whereas myosin II was organized into laterally associated, head-

293 sing mathematical modeling for Dictyostelium myosin II, we predict that myosin II mechanoresponsivene

294 al accumulation of Rho kinase and non-muscle myosin II, which coordinate apical constriction.

295 on in myo2-S1 affects the activation loop of Myosin II, which is involved in physical interaction wit

296 ions produce force-dependent accumulation of myosin II, which is thought to be responsible for their

297 dherin induces an asymmetric accumulation of Myosin-II, which leads to a highly contractile cell inte

298 ng actin with latrunculin A or by inhibiting myosin II with blebbistatin).

299 Interactions of myosin-II with actin filaments produce force to assemble

300 CR), the precise ultrastructure of actin and myosin II within the animal cell CR remains an unanswere