ライフサイエンスコーパス: myosin

1 HC and blebbistatin bind to the same site on myosin.

2 s also results in accumulation of junctional myosin.

3 myosin and decreased by >3-fold for the fast myosin.

4 ified between tropomyosin and both actin and myosin.

5 tional differences in Drosophila EMB and IFI myosins.

6 e in opposite directions while also shedding myosins.

7 Myosin-1C is a single-headed, short-tailed member of the

8 ion of the individual kinetic steps of human myosin-1C isoforms in their productive interaction with

9 fold changes in the maximum power output per myosin-1C motor and 4-fold changes in the velocity and t

10 w that PH domains occur in all Dictyostelium myosin 1s and that the BH sites of Myo1A, B, C, D, and F

11 -hydrophobic (BH) sites but the mechanism of myosin 1s distinctive lipid targeting is poorly understo

12 All myosin 1s except Myo1A are present in macropinocytic str

13 a similar role in the localization of other myosin 1s.

14 own structure is relevant to all isoforms of myosin-2 and provides a framework for understanding thei

15 Myosin-2 is essential for processes as diverse as cell d

16 Treatment with 4-HAP activates nonmuscle myosin-2C (NM2C) (MYH14) to alter actin organization, in

17 Here we identify nonmuscle myosin-2C (NM2C) as a component of the terminal web.

18 freezing rate caused appearance of a 160 kDa myosin-4 fragment in SDS-PAGE, further decreased water-h

19 villar adhesion complex is homologous to the myosin-7a (MYO7A)-based Usher syndrome complex and Choi

20 o has important implications for research on myosin-7a and hereditary deaf-blindness.

21 i et al. also report that CALML4 can bind to myosin-7a, this work also has important implications for

22 ted knockout screen, we identify SLC35B2 and myosin-7B (MYO7B) as critical endocytosis regulators for

23 lex based on cadherins and the motor protein myosin-7b (MYO7B) links the tips of intestinal microvill

24 n complex and functions as a light chain for myosin-7b.

25 direct binding partner of the IMAC component myosin-7b.

26 r sizes leading to clotting disorders termed myosin-9-related disorders (MYH9-RDs).

27 the glideosome is an essential and divergent Myosin A motor (PfMyoA), a first order drug target again

28 en myosin-induced flow and advection-induced myosin accumulation, which leads to clustering and local

29 sts that in animals, as in yeast and plants, myosin/actin can drive long-range transport.

30 theca to study the mechanisms of coordinated myosin activation in vivo.

31 ys and how their phosphorylation would allow myosin activation.

32 cle 2-deoxy-ATP (dATP) was used to study how myosin activators may affect soleus muscle relaxation.

33 Thus, TNT1 may modulate acto-myosin activity by optimizing F-actin-tropomyosin interf

34 Recent studies highlight that alongside myosin activity, cortical actin organization is a key re

35 mally induced by pharmacologic inhibition of myosin activity.

36 tion increases the fluorescence 20-fold, how myosin and cofilin binding to filaments reduces the fluo

37 velocity increased by ~10-fold for the slow myosin and decreased by >3-fold for the fast myosin.

38 old question on the function of terminal web myosin and hold broad implications for understanding api

39 Because actin is more highly conserved than myosin and most other muscle proteins, most such efforts

40 Actin's interactions with myosin and other actin-binding proteins are essential fo

41 o other cytoskeleton proteins such as actin, myosin, and tubulin.

42 the actin- and nucleotide-binding regions of myosin assures a proper actin-binding interface and acti

43 f actomyosin contractility (specifically, of myosin ATPase, Rho kinase, or myosin light-chain kinase

44 Inhibitors of muscle myosin ATPases are needed to treat conditions that could

45 (2020) describe a nuclear actin-myosin-based pathway driving the movement of activated g

46 int and provides testable predictions of new myosin behaviors, including the stomp distribution and t

47 Myosin, beta-enolase, CK-M-type and actin were identifie

48 ibitory position on F-actin, where it deters myosin binding at rest, and that, correspondingly, cross

49 We confirm that the nine stripes ascribed to myosin binding protein-C are not related to the titin se

50 ded] N'-terminal domains C0 to C7 of cardiac myosin binding protein-C) fragment and an insoluble C'-t

51 ant] N'-terminal domains C0 to C7 of cardiac myosin binding protein-C)-sc returned pCa(50) and k(tr)

52 e confined to the filament domain containing myosin binding protein-C, the "C-zone." Myosin motors in

53 n filament surface, which uncovers or blocks myosin binding sites along F-actin.

54 re all in positions that would hinder strong myosin binding to actin.

55 Cardiac myosin-binding protein-C (cMyBP-C) is highly phosphoryla

56 a function of Ca(2+) to regulate exposure of myosin-binding sites and, thus, myosin cross-bridge recr

57 Targeting skeletal muscle myosin by MPH-220 enabled muscle relaxation, in human an

58 , and intracellular proteins and organelles, myosins can generate contractility, directly regulate ac

59 e exon-encoded regions within the Drosophila myosin catalytic domain.

60 nd biological tools facilitates the study of myosin-chaperone interactions in mechanistic detail.

61 a single-headed, short-tailed member of the myosin class I subfamily that supports a variety of acti

62 =12-fold) for skeletal myosin versus cardiac myosin compared to BHC.

63 aalpha-tropomyosin, and masseter muscle beta-myosin complexes; masseter myosin, which shares sequence

64 c structure of MPH-220-bound skeletal muscle myosin confirmed the mechanism of specificity.

65 Myosin conformations establish work-energy equipoise tha

66 For the dimerization, we reconstitute acto-myosin connection of a tailless E-cadherin by two ways:

67 Our approach employs a chimeric myosin consisting of the MYO10 motor domain fused to the

68 kingly, when titin-cleaved muscles contract, myosin-containing A-bands become split and adjacent myos

69 titin is closely associated with the thick, myosin-containing filament and exhibits a complex patter

70 h I region of the active site to examine how myosin couples structural changes in the actin- and nucl

71 regulated by Ca(2+) -dependent modulation of myosin cross-bridge binding to F-actin by the thin filam

72 exposure of myosin-binding sites and, thus, myosin cross-bridge recruitment and force production.

73 In a contracting muscle, myosin cross-bridges extending from thick filaments pull

74 re given Lactobacillus casei over-expressing myosin-cross-reactive antigen (LC(+mcra)).

75 ll polarity in the organisation of the actin-myosin cytoskeleton and is postulated to reflect directi

76 To estimate the rate of myosin deactivation, we followed the rate of the intensi

77 Posteriorly positioned myosin-dependent contractile forces pull on cell-cell co

78 The myosin-directed chaperone UNC-45B is essential for sarco

79 analytical results shed new light on in-bulk myosin-driven cell motility in living cells and provide

80 The motor protein myosin drives muscle and nonmuscle motility by binding t

81 Destabilization of myosin energy-conserving states promotes contractile abn

82 Myosin ensembles have been modeled via several strategie

83 lopment in airway SM tissue by catalysing NM myosin filament assembly, and that the interaction of S1

84 on of airway SM contraction by catalysing NM myosin filament assembly.

85 irway SM at the cell cortex and catalysed NM myosin filament assembly.

86 dynamic cellular functions of NMII, such as myosin filament formation and nascent adhesion assembly,

87 Myosin filament stress-sensing determines the strength a

88 in vitro of nonphosphorylated smooth muscle myosin filaments by the addition of MgATP is the reverse

89 n networks, buffering the forces observed by myosin filaments during contraction.

90 containing A-bands become split and adjacent myosin filaments move in opposite directions while also

91 y unstudied affinity of skeletal and cardiac myosin for phospholipid membranes.

92 sing genetic and biochemical manipulation of myosins, force measurement techniques, and live-cell ima

93 After 4 h, the myosins form thick bipolar and, for smooth muscle myosin

94 With SRX myosin found predominantly in the C-zone, these data sug

95 mally found between actin and tropomyosin on myosin-free thin filaments in relaxed muscle, thus restr

96 se that RLCs are crucial for fine-tuning the myosin function.

97 e advanced our understanding of how specific myosins function at individual steps of phagocytosis.

98 Myosins generate force and motion by precisely coordinat

99 ion by ~1:100 000 TF/myosin, whereas cardiac myosin had TF-like activity >10-fold higher.

100 to the actin filament between the tip of the myosin head and a cleft on the innermost edge of actin s

101 dence for the predicted ensemble behavior of myosin head domains.

102 population, suggesting that mavacamten-bound myosin heads are not permanently protected in the SRX st

103 on fall was caused by detachment of M.ADP.Pi myosin heads from actin and reversal of the first tensio

104 With dATP, myosin heads may remain in an activated state near the t

105 tended closer to actin in relaxed muscle and myosin heads return to an ordered, resting state after c

106 gest that dATP induces structural changes in myosin heads that increase the surface area of the actin

107 ce relative to WT muscle while the return of myosin heads to an ordered resting state was initially s

108 ction data indicate that with elevated dATP, myosin heads were extended closer to actin in relaxed mu

109 evidence indicates that with elevated dATP, myosin heads were extended closer to actin in resting mu

110 One outstanding question is whether the myosin heavy chain (MHC) isoforms alone account for thes

111 Myosin heavy chain (MHC) isoforms in goat muscles and th

112 myogenesis that inhibit transcription of the myosin heavy chain (MHC) protein family.

113 on index and myotube diameter; likewise, the myosin heavy chain (MyHC)-IIB isoform (encoded by Myh4)

114 muscle (ASM) against a loss of smooth muscle myosin heavy chain (SMMHC) expression.

115 fibers, which express a slow fiber-specific myosin heavy chain 1 (Smyhc1), are the first group of mu

116 methylation status of the pivotal VSMC gene myosin heavy chain 11 (Myh11).

117 ense variants in the MYH7-encoded MYH7 (beta myosin heavy chain 7) represent a leading cause of hyper

118 Also, SOD1 myotubes had loosely arranged myosin heavy chain and reduced acetylcholine receptor ex

119 vation domains under the control of the Myh (myosin heavy chain) 6 promoter was generated.

120 expression of JunD via the alpha MHC (alpha- myosin heavy chain) promoter (alpha MHC JunD(tg)) were p

121 ) stimulated the binding of S100A4 to the NM myosin heavy chain, which was catalysed by RhoA GTPase v

122 Myosin heavy chain-embryonic (MyHC-emb) is a skeletal mu

123 1 CM-specific knockout (KO) mice using alpha-Myosin Heavy Chain-nuclear Cre (ZO-1cKO) and investigate

124 olabelling muscle biopsies for developmental myosin heavy chain.

125 We show that myo-sex, a myosin heavy-chain gene also in the M-locus, was require

126 h shares sequence identity with beta-cardiac myosin-heavy chain, was used because of its stability in

127 Myosin-IC (Myo1c) has been proposed to function in deliv

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

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

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

131 ROCK-myosin II ablation specifically kills resistant cells vi

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

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

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

135 nduced by perturbations that alter nonmuscle myosin II activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Myosin II is the motor protein that enables muscle cells

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

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

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

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

156 NM myosin II undergoes polymerization in airway SM and regu

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

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

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

160 as previously discovered to inhibit skeletal myosin II.

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

162 traction of the resultant actin filaments by myosin II.

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

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

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

166 Nonmuscle myosin IIA (NMIIA) heavy chain gene (MYH9) mutations cau

167 nds on the contractile activity of nonmuscle myosin IIA (NMIIA) motor proteins.

168 tes the dynamic redistribution of non-muscle myosin IIA and beta2-integrin, which facilitate neutroph

169 ociated actin regulatory proteins, including myosin IIA and ezrin, and that these effects are depende

170 Myosin IIA promoted internalization of MHCI and myosin I

171 ell center through the dynamic shortening of myosin IIA-associated actin stress fibers to drive rapid

172 sin IIA promoted internalization of MHCI and myosin IIB drove CD59 uptake in both HeLa and polarized

173 v mecarbil (OM)-a novel activator of cardiac myosin-improves left ventricular systolic function and r

174 stimulation causes the polymerization of NM myosin in airway SM, which is necessary for tension deve

175 We end the review by describing the roles of myosin in parasites and the therapeutic potential of tar

176 , and that the interaction of S100A4 with NM myosin in response to contractile stimulation is activat

177 Curling originates from an enrichment of myosin in the basal domain that generates an active spon

178 In this report, we show that myosins in STFs mirror the more electrostatic and cooper

179 ilized these and increased the proportion of myosins in the DRX conformation, which enhanced cardiomy

180 Hibernation increased the proportion of myosins in the SRX conformation, whereas pathogenic vari

181 processing lies near the phagocytic cup in a myosin-independent fashion.

182 scle, thus restructuring the filament during myosin-induced activation.

183 contraction mediates a feedback loop between myosin-induced flow and advection-induced myosin accumul

184 erativity between actin filament severing by myosin-induced forces and by gelsolin.

185 Direct myosin inhibition could provide optimal muscle relaxatio

186 sting a first-in-class, targeted strategy of myosin inhibition to improve symptom burden and exercise

187 scale with the adhesion energy, while actin/myosin inhibitions strongly reduce the uptake frequency,

188 fety of mavacamten, a first-in-class cardiac myosin inhibitor, in symptomatic obstructive hypertrophi

189 Mavacamten, a novel myosin inhibitor, was well tolerated in most subjects wi

190 In relaxed muscle, the two heads of myosin interact with each other on the filament surface

191 Although the structural basis of actin and Myosin interaction is revealed at a quasiatomic resoluti

192 vel elucidation of tropomyosin regulation of myosin interaction with actin in muscle contraction, and

193 area of the actin-binding regions promoting myosin interaction with actin, which could explain the o

194 area of the actin-binding regions, promoting myosin interaction with actin.

195 ntial for the proper folding and assembly of myosin into muscle thick filaments in vivo.

196 scle relaxation; however, targeting skeletal myosin is particularly challenging because of its simila

197 the mechanical output of both slow and fast myosins is sensitive to the RLC isoform.

198 werful system for characterizing alternative myosin isoforms and modeling muscle diseases, but high-r

199 Pharmacological control of myosin isoforms is a promising approach to address metas

200 ified a key residue difference between these myosin isoforms, located in the communication center of

201 of the intensity recovery of the first-order myosin layer line (MLL1) and restoration of the resting

202 h increased JNK2 phosphorylation and reduced myosin light chain (MLC(20) ) phosphorylation.

203 Myosin light chain (MYL1 and MYL3) showed high oxidative

204 Confocal images of phospho-myosin light chain (pMLC) immunofluorescence, moreover,

205 d that active RhoA and ROCK effector phospho-myosin light chain (pMLC) were downregulated in endothel

206 antly decreased in MetSyn lymphatic vessels, myosin light chain 20, MLC(20) phosphorylation was incre

207 abnormal phenotypes in both models of MYL4 (myosin light chain 4)-related atrial cardiomyopathy.

208 rease in permeability via phosphorylation of myosin light chain and subsequent shrinkage of human bra

209 tro and in vivo, the precise role of cardiac myosin light chain kinase (cMLCK), the primary kinase ac

210 ts the CaM binding domain of skeletal muscle myosin light chain kinase, forms a complex with CaM in t

211 on by blocking the nuclear factor-kappaB and myosin light chain kinase-mediated redistribution of the

212 ls regulate blood-brain barrier function via myosin light chain phosphorylation and increase in perme

213 ction and lower expression of phosphorylated myosin light chain.

214 ecifically, of myosin ATPase, Rho kinase, or myosin light-chain kinase activity).

215 the contractile force generated by actin and myosin linked to the plasma membrane at cell-cell and ce

216 Depletion of Lfc leads to aberrant myosin localization, thereby causing two effects that ra

217 This study of the dATP-induced changes in myosin may be instructive for determining the structural

218 he thick filament and the arrangement of the myosin motor domains.

219 protein melanophilin of the actin-associated myosin motor is one such "shared protein," which also in

220 stimulated trafficking of GLUT4 requires the myosin motor Myo1C and signaling adaptor 14-3-3beta.

221 trapping and biochemical reconstitution with myosin motor proteins to show single piconewton forces a

222 ive torques generated by the polarization of myosin motors along their apicobasal axis.

223 Inactivated myosin motors are folded against the filament core, and

224 hortening in the muscle sarcomere are due to myosin motors from thick filaments pulling nearby actin

225 ning myosin binding protein-C, the "C-zone." Myosin motors in domains further from the filament midpo

226 s driven by contractile tension generated by myosin motors in the sub-membranous actin cortex.

227 We show that, although myosin motors throughout the filament contribute to forc

228 erence-based knockdown of the unconventional myosin Myo16 in cortical neurons altered growth cone fil

229 ing microscopy to investigate a minimal acto-myosin network linked to a supported lipid bilayer membr

230 cent work has shown that the remodeling acto-myosin network modifies local membrane organization, but

231 emodeling to a contractile state of the acto-myosin network.

232 e and exhibits structural features common to myosins of diverse classes from all kingdoms of life.

233 ed with the furrow region, none of the three myosins (of types VIII and XI) is localized there.

234 Furthermore, when relaxed, myosin partition into two kinetically distinct subpopula

235 g of S100A4 to NM myosin was required for NM myosin polymerization, adhesome assembly and actin polym

236 asked whether contaminating phospholipid in myosin preparations may also contain tissue factor (TF).

237 Myosin protein was exposed to diazinon and chlorpyrifos

238 Further, skeletal myosin provides membrane-like support for activated prot

239 Although myosin regulatory light chain (RLC) phosphorylation has

240 The fast skeletal myosin regulatory light chain 2 followed by other five i

241 minating phospholipid is required to support myosin-related prothrombinase activity.

242 ing site for glucans and also interacts with MYOSIN-RESEMBLING CHLOROPLAST PROTEIN, a proposed struct

243 ises the question of whether purified muscle myosins retain procoagulant phospholipid through purific

244 in the temperature range of 50-55 degrees C (myosin rod denaturation).

245 nucleoside triphosphate, we demonstrate that myosin's force- and motion-generating capacity can be dr

246 insic control by affecting distinct steps in myosin's mechanochemical cycle.

247 ogenic electron microscopy reconstruction of myosin-S1-decorated F-actin-tropomyosin together with at

248 In the myosin-saturated state of the thin filament, there is a

249 ns form thick bipolar and, for smooth muscle myosin, side-polar filaments.

250 weakens mavacamten's ability to increase the myosin SRX population, suggesting that mavacamten-bound

251 able tool to provide novel insights into the myosin SRX state in healthy, diseased, and therapeutic c

252 In noncontracting, "relaxed" muscle, myosin still hydrolyzes ATP slowly, contributing to the

253 sin subfragments, heavy meromyosin (HMM) and myosin subfragment 1 (S1).

254 SRX) state, which are not seen using shorter myosin subfragments, heavy meromyosin (HMM) and myosin s

255 lar dynamics simulations of post-powerstroke myosin suggest that dATP induces structural changes in m

256 lar dynamics simulations of post-powerstroke myosin suggest that dATP induces structural changes in m

257 Skeletal myosin supported factor VIIa cleavage of factor X equiva

258 exin A5 and phospholipase A2 blocked >95% of myosin-supported activity, confirming that contaminating

259 ructural changes desired for other potential myosin-targeted molecular compounds to treat muscle dise

260 During activation, combinations of cycling myosin that contribute insufficient activation energy de

261 gest that dATP induces structural changes in myosin that increase the surface area of the actin-bindi

262 these systems, which is the molecular motor myosin that moves on tracks of filamentous (F-) actin.

263 for adenosine triphosphate (ATP) turnover by myosin, the actomyosin system and for insoluble, high mo

264 es show that pathogenic missense variants in myosin, the molecular motor of the sarcomere, are cluste

265 e first x-ray crystal structure of an insect myosin: the D melanogaster skeletal muscle myosin II emb

266 Depending on the myosin turnover rate, junctions either preserve stable l

267 Myosins undergo physiological shifts between the SRX con

268 Proteins, among which heavy chain myosin, underwent denaturation and aggregation, as shown

269 hensive analytical and numerical modeling of myosin V diffusion and stepping.

270 This transport requires a myosin V motor, Myo2, which attaches to the vacuole via

271 y using a dominant negative approach against myosin V, spine synapses became stronger compared to con

272 /Staufen from the cortex along microtubules, myosin-V anchors osk/Staufen at the cortex.

273 In budding yeast, the myosin-V Myo2 is aided by the kinesin-related protein Sm

274 Myosin-V wins over kinesin-1 at the posterior pole due t

275 tubule motor, kinesin-1, and an actin motor, myosin-V, are essential for osk mRNA posterior localizat

276 For molecular motors such as myosin-V, the ratio of forward to backward steps and the

277 e recently discovered that the motor protein myosin-Va works with dynamic actin tracks to drive long-

278 Thus, in addition to melanophilin/myosin-Va, Rab27a can recruit SPIREs to melanosomes, the

279 rmin-1 to generate actin tracks required for myosin-Va-dependent transport in melanocytes.

280 We then tested whether the positions of myosin variants of unknown clinical significance that we

281 ) is caused by inactivating mutations in the myosin VB gene (MYO5B).

282 uM) and selectivity (>=12-fold) for skeletal myosin versus cardiac myosin compared to BHC.

283 Myosin VI is involved in many cellular processes ranging

284 nce length of more than 200 angstrom for the myosin VI SAH domain.

285 is interaction blocks the ability of nuclear myosin VI to bind DNA and its transcriptional activity i

286 We apply the theory to myosin VI, a motor that takes frequent backward steps an

287 competition affects the activity of nuclear myosin VI, we demonstrate the impact of a concentration-

288 oss of DAB2, a tumor suppressor, may enhance myosin VI-mediated transcription.

289 Motor activity of nuclear myosin was dependent on the Hsp90 chaperone.

290 The binding of S100A4 to NM myosin was required for NM myosin polymerization, adheso

291 es associated with dominant DA interact with myosin whereas the residues altered in families with rec

292 equivalent to contamination by ~1:100 000 TF/myosin, whereas cardiac myosin had TF-like activity >10-

293 seter muscle beta-myosin complexes; masseter myosin, which shares sequence identity with beta-cardiac

294 ination of the mechanics and kinetics of the myosin working stroke with a smaller set of data.

295 wo gene families, the actin-dependent motor, myosin XI (a,b), and the putative chitin receptor Lyk5 (

296 Rab-E co-localises with myosin XI at sites of active exocytosis, and at the grow

297 plant growth in P. patens and the rab-E and myosin XI phenotypes are rescued by A. thaliana's Rab-E1

298 y corresponded to a maximal 93% reduction of myosin XI protein and complete loss of chitin-induced ca

299 re known about how molecular motors, such as myosin XI, associate with their secretory cargo to suppo

300 pes are rescued by A. thaliana's Rab-E1c and myosin XI-K/E, respectively.