ライフサイエンスコーパス: exocyst

1 etory vesicles where they act to recruit the exocyst.

2 f both Ral GTPases were mediated through the exocyst.

3 sma membrane is a protein complex called the exocyst.

4 Ciliogenesis and cystogenesis require the exocyst, a conserved eight-protein trafficking complex t

5 The exocyst, a conserved multiprotein complex, tethers secre

6 Gain of function of the exocyst, a conserved protein complex involved in tetheri

7 Here, we show that the exocyst, a conserved protein complex that facilitates do

8 The exocyst, a eukaryotic tethering complex, coregulates tar

9 We demonstrated previously that the exocyst, a highly conserved eight-protein membrane traff

10 Bodemann et al. now show that the exocyst, a protein complex involved in tethering transpo

11 Sec5 is a subunit of the exocyst, a protein complex that is involved in vesicle t

12 We previously showed that the exocyst, a protein trafficking complex, is essential for

13 and temporal dynamics of exocytosis via the exocyst, a putative tethering protein complex.

14 A third Rab GTPase, Sec4, and the exocyst act in tethering and fusion of these vesicles.

15 The Sec3 subunit of the exocyst acts as a spatial landmark for exocytosis throug

16 We previously localized the exocyst, an eight-protein complex involved in membrane t

17 es before membrane fusion is mediated by the exocyst, an essential phylogenetically conserved octamer

18 abin8 interacts with Sec15, a subunit of the exocyst and downstream effector of Rab8.

19 og4 bears a strong structural resemblance to exocyst and Dsl1p complex subunits.

20 itment of both recycling endosome-associated Exocyst and ESCRT machinery during late telophase, and t

21 ly through SipC-dependent recruitment of the exocyst and indirectly via SopE-dependent activation of

22 We observe sub-complexes in exocyst and intraflagellar transport complexes, which we

23 ine the functional relationships between the exocyst and PAR proteins, we show that RAL-1 recruits th

24 gative mutant of Rab8a strongly binds to the exocyst and prevents recruitment to the bladder, suggest

25 te directs exocytosis of lysosomes using the exocyst and SNARE SNAP-29 to form a large protrusion tha

26 uggested functional interactions between the exocyst and the DDR.

27 We conclude that the exocyst and TRAPP-II complex have distinct localizations

28 s for complexes without known structure (the exocyst and tRNA multi-synthetase complex) and by establ

29 o subunits of other MTCs including the Dsl1, exocyst, and Golgi-associated retrograde protein (GARP)

30 dicate that assembly and polarization of the exocyst are functionally separable events, and that Sec6

31 We found that WASH and exocyst are required for matrix degradation by an exocyt

32 s with high invasion potential; blocking the exocyst-Arp2/3 interaction inhibited Arp2/3-mediated act

33 Our studies also implicate the exocyst as a Rab11 effector in this process and that Rab

34 with Sec15 uncovers additional roles for the exocyst as an adaptor for molecular motors and implies s

35 is proposed to release Sec9 in favor of Sec6-exocyst assembly and to simultaneously recruit Sec1 to s

36 for the synthetic lethal interactions or the exocyst assembly defects.

37 Elucidating the mechanisms regulating exocyst assembly is important for the understanding of e

38 Exocyst assembly requires activation of the small GTPase

39 lusive of Sec6-Sec9 but compatible with Sec6-exocyst assembly.

40 omotes RhoA activation, which then regulates exocyst assembly/localization and exocytosis.

41 Exo70 targeting and orient the tethering of exocyst-associated E-cadherin.

42 nization of microtubules, and trafficking of exocyst-associated membranes.

43 the small GTPase Cdc42 co-localizes with the exocyst at primary cilia and interacts with the exocyst

44 e Rab11 GTP-activating protein Evi5, and the exocyst at the mother centriole.

45 e Cdc42 is a candidate for regulation of the exocyst at the primary cilium.

46 TP-bound form of Arl13b, consistent with the exocyst being an effector of Arl13b.

47 Indeed, disruption of GRIP1-exocyst binding caused a strikingly similar deficit in A

48 Exocyst biogenesis is regulated by several processes, bu

49 e direct phosphorylation of a subunit of the exocyst by a specific cyclin-dependent kinase complex.

50 is coordinated disruption of the Rab11/Sec15 exocyst by anthrax toxins may contribute to toxin-depend

51 cretory canal and other polarized cells, the exocyst co-localizes with the PAR polarity proteins PAR-

52 Par3 and the exocyst colocalized by immunofluorescence and coimmunopr

53 In a 3T3-L1 adipocyte cell line, the Exocyst complex and its Exo70 subunit were shown to crit

54 Here, we describe an interaction between the exocyst complex and the endosomal Arp2/3 activator Wisko

55 e tethering complexes, such as Sec6 from the exocyst complex and Vps53 from the Golgi-associated retr

56 hus, this work implicates a fully functional exocyst complex as a component of the compatible pollen

57 Systems analysis identified the exocyst complex as a key network hub, rich in genetic in

58 We demonstrate that organization of the exocyst complex at the appressorium pore is a septin-dep

59 was not required for the accumulation of the exocyst complex at the midbody.

60 olysis and requires vesicle tethering by the exocyst complex but does not require vesicle fusion with

61 e 11 open reading frame (C11orf30/EMSY), and exocyst complex component 4 (EXOC4) reached a threshold

62 g the small GTPases Cdc42 and Arl13b and the exocyst complex component Sec6.

63 nd RAB27b are recruited and activated by the exocyst complex components SEC6/SEC15.

64 izing enzyme, PIPKIgammai2, in regulation of exocyst complex control of cell polarity and polarized i

65 a temporal interaction between Cdc42 and the exocyst complex during large particle uptake.

66 ereby establishing a functional role for the exocyst complex during phagocytosis.

67 tly phosphorylated Exo84, a component of the exocyst complex essential for exocytosis.

68 tical role in this process by mobilizing the exocyst complex for GLUT4 vesicle targeting in adipocyte

69 h, increased migration, and dysregulation of exocyst complex formation.

70 Here, we investigated the functions of exocyst complex genes encoding the remaining seven subun

71 components and promotes the assembly of the exocyst complex in response to epidermal growth factor (

72 cular dissection of the GTPase Rab8a and the exocyst complex in tethering of the contractile vacuole

73 support of a function for a Sec3-containing Exocyst complex in the assembly or maintenance of desmos

74 les of Ral GTPases and their common effector exocyst complex in the formation of nascent TJs.

75 ) generation controls the integration of the exocyst complex into an integrin-containing trafficking

76 ent evidence that the Exo70 component of the exocyst complex is a direct effector of both Rho3 and Cd

77 The EXOCYST complex is central to this process, and in yeast

78 ing this allele, we investigated whether the exocyst complex is required for cellularization.

79 The exocyst complex is required for some, but not all, forms

80 The exocyst complex is required for tethering of secretory v

81 determined that the presence of an octameric exocyst complex is required for the formation of a funct

82 Here, we show that the exocyst complex localizes to the tips of growing hyphae

83 The assembly of the exocyst complex mediates the tethering of post-Golgi sec

84 e expression of phosphorylated ERK, p21, and exocyst complex members Sec8 and Sec10, in the remaining

85 boration is coordinated by deposition of the exocyst complex on bacteria-containing vesicles, an even

86 The exocyst complex plays a critical role in targeting and t

87 nents Sec3, Sec5, Sec6, Sec8, and Sec15, and exocyst complex proteins Exo70 and Exo84 localize specif

88 The exocyst complex regulates the last steps of exocytosis,

89 The exocyst complex seems to achieve this spatial regulation

90 plasma membrane, possibly forming different exocyst complex subpopulations.

91 Sec5, which is an exocyst complex subunit and localizes to ingressing furr

92 t Rab8 behaviors require the function of the exocyst complex subunit Sec5 as well as the recycling en

93 abidopsis thaliana Exo70B2, a subunit of the exocyst complex that mediates vesicle tethering during e

94 Here we report that Sec3, a component of the exocyst complex that mediates vesicle tethering during e

95 , for localization of the GTPase Ral and the exocyst complex to this region.

96 ction by disrupting the interaction with the exocyst complex via Sec15p.

97 The exocyst complex was believed to target and tether post-G

98 he Sec4p effector Sec15p (a component of the exocyst complex) compete for binding to Sec2p.

99 These functions do not involve the exocyst complex, a common Ral guanosine triphosphatase (

100 ladder epithelial cells (BECs) mobilized the exocyst complex, a powerful exporter of subcellular vesi

101 The exocyst complex, an effector of Rho and Rab GTPases, is

102 ruits Drainin, a Rab11a effector, Rab8a, the exocyst complex, and LvsA, a protein of the Chediak-Higa

103 racts with Sec10, a crucial component of the exocyst complex, and that Cdc42 colocalizes with Sec10 a

104 focused on exoc5, a central component of the exocyst complex, by analyzing both exoc5 zebrafish mutan

105 ctivation of Sec10, a central subunit of the exocyst complex, in the epithelial cells of the ureter a

106 e demonstrate that Exo70, a component of the exocyst complex, induces tubular membrane invaginations

107 (exocyst component of 70 kDa) subunit of the exocyst complex, resulting in inhibition of exocytosis a

108 Myrip also interacts with actin and the exocyst complex, suggesting that it may exert multiple r

109 y, which stretches from Rab8 to RalA and the exocyst complex, that mediates rapid furrow formation in

110 ation of Exo84 disrupted the assembly of the exocyst complex, thereby affecting exocytosis and cell s

111 Here, we show that Exo70, a component of the exocyst complex, undergoes isoform switching mediated by

112 n between SipC and Exo70, a component of the exocyst complex, which mediates docking and fusion of ex

113 assemble fluorescently tagged Sec8 into the exocyst complex, which was shown to be functional by bio

114 n-2 are dependent on IFT20, GMAP210, and the exocyst complex, while smoothened delivery is largely in

115 ge factor Sec2p regulate the assembly of the exocyst complex.

116 g axons expands in a process mediated by the exocyst complex.

117 s nuclear membrane expansion, actin, and the exocyst complex.

118 ion with RalBP1/RLIP76 and components of the exocyst complex.

119 bly as a regulator of exocytosis outside the exocyst complex.

120 proteins, the Sec5 and Exo84 subunits of the exocyst complex.

121 pendent membrane raft exocytosis through the exocyst complex.

122 clustering in hotspots depend on the intact exocyst complex.

123 (GEF) that precipitated the assembly of the exocyst complex.

124 Our data support the concept that the exocyst-complex subunits dynamically dock and undock at

125 In mammalian epithelial cells, Exocyst complexes are recruited to nascent sites of cell

126 events, and that Sec6p is required to anchor exocyst complexes at sites of secretion.

127 These results suggest that two different exocyst complexes may function in basal-lateral membrane

128 e show that Sec3 associates with a subset of Exocyst complexes that are enriched at desmosomes.

129 ains regulated by different EXO70-containing exocyst complexes within a single cell.

130 ing requires cooperation between the PAR and exocyst complexes.

131 Here we show that the exocyst component Exo70 is a direct substrate of the ext

132 With RNAi knockdown of the exocyst component Exo70 or Sec8, MDA-MB-231 cells expres

133 In S. cerevisiae, phosphorylation of the exocyst component Exo84 by Cdk1-Clb2 during mitosis caus

134 d that STK38 supports the interaction of the exocyst component Exo84 with Beclin1 and RalB, which is

135 olecule Endosidin2 (ES2) binds to the EXO70 (exocyst component of 70 kDa) subunit of the exocyst comp

136 cyst at primary cilia and interacts with the exocyst component Sec10.

137 d was accompanied by the polarization of the exocyst component Sec15.

138 mechanism unrelated to its interaction with exocyst component Sec15p.

139 We demonstrate that the N terminus of the exocyst component Sec3 directly interacts with phosphati

140 s the destruction of the formin Bni1 and the exocyst component Sec3.

141 culum to perinuclear vesicles containing the exocyst component Sec5 (also known as EXOC2).

142 SSR growth requires Ral and the exocyst component Sec5 and Ral-induced enlargement of th

143 ngly, we found that GEF-H1 directly binds to exocyst component Sec5 in a Ral GTPase-dependent manner.

144 ased RalB association with its effector, the exocyst component Sec5.

145 RalA interaction with the Exo84 but not Sec5 exocyst component was necessary for supporting anchorage

146 ho3p-interacting proteins, such as Sec8p, an exocyst component, Apm1p, a subunit of the clathrin adap

147 icles with Myo2p, the GEF Sec2p, and several exocyst components allowed us to document a timeline for

148 ation enhances the binding of Exo70 to other exocyst components and promotes the assembly of the exoc

149 ted with a novel form of secretion involving exocyst components and the Sso1 t-SNARE.

150 Although most exocyst components are brought to these sites by riding

151 mutated in cells impair the localization of exocyst components at the plasma membrane and lead to de

152 Here, we show that exocyst components coprecipitate with SipC and accumulat

153 , or conditional mutation, of genes encoding exocyst components leads to impaired plant infection.

154 with the outer macrovesicular layer, whereas exocyst components SEC-5, -6, -8, and -15 form a delimit

155 The exocyst components Sec3, Sec5, Sec6, Sec8, and Sec15, an

156 ment of the Rab GTPase Sec4p, as well as the exocyst components Sec3p and Sec8p, to the precursor ves

157 sion but occurs later than that of the known Exocyst components Sec6 and Sec8 that are recruited to a

158 ible redundancy with Sec3p and Sec15p, other exocyst components that also interact with polarity dete

159 and multisubunit tethering complexes such as exocyst, conserved oligomeric Golgi complex, Golgi-assoc

160 We find that exocyst-deficient terminal cells have highly truncated b

161 6S proteasome subunit, Rpt2, indicating that exocyst degradation is controlled by the ubiquitin-prote

162 Here, to unravel the components of the exocyst degradation pathway, we screened for extragenic

163 ear membrane expansion, DNA replication, and exocyst-dependent anchoring of the nuclear envelope to t

164 used RalB-selective activation and Sec5- and exocyst-dependent engagement of mTORC1 and suppression o

165 rons increases dendritic spine density in an exocyst-dependent manner and increases Sec5 in spines.

166 ound that STK38 is stimulated in a MOB1- and exocyst-dependent manner.

167 ctivates AKT normally, but AKT activation by exocyst-dependent mechanisms is impaired.

168 These findings reveal that RAL-1 and the exocyst direct the polarized vesicle fusion events requi

169 whereas Sec2p and all the components of the exocyst disperse coincident with fusion.

170 inds directly to Exo70 and is sufficient for exocyst docking, membrane-protein delivery and cell surv

171 dent on RalBP1/RLIP76 but not Sec5 and Exo84 exocyst effector function.

172 A component of the exocyst, Exo70, directly interacts with the Arp2/3 compl

173 using short hairpin RNA (shRNA) to knockdown exocyst expression and stable transfection to induce exo

174 Exocyst foci partially overlapped with vesicles visualiz

175 Exocyst foci were independent of cytoskeleton, although

176 ur findings provide a mechanism by which the exocyst function and actin dynamics are modulated for EM

177 Disrupting the exocyst function by siEXO70 or siSEC8 treatment or by ex

178 Furthermore, disruption of exocyst function through Exo70 depletion led to a defect

179 er, our results indicate that Arl13b and the exocyst function together in the same pathway leading to

180 associate with the cortex but cannot support exocyst function.

181 nthesis of TC10, a small GTPase required for exocyst function.

182 ug treatments, supporting the concept of the exocyst functioning as a dynamic particle.

183 re consistent with an important role for the exocyst in coordinating endocytosis and exocytosis.

184 complex assembly, and uncovers a role of the exocyst in promoting membrane fusion in addition to vesi

185 recipitation, consistent with a role for the exocyst in targeting and docking vesicles carrying prote

186 mponents of the DNA damage response (DDR) as exocyst-interacting proteins, together with the identifi

187 In contrast, the Sec6-exocyst interaction is incompatible with Sec6-Sec9.

188 We have also found that the exocyst interacts with the Arp2/3 complex in cells with

189 The Exocyst is a conserved multisubunit complex involved in

190 The exocyst is a heterooctomeric complex well appreciated fo

191 interaction with the Exo70 component of the exocyst is a key event in spatial regulation of exocytos

192 The exocyst is a multiprotein complex essential for exocytos

193 polarized membrane traffic regulated by the exocyst is an essential component of cell migration and

194 The exocyst is an essential component of the secretory pathw

195 The exocyst is an evolutionarily conserved octameric complex

196 The exocyst is an octameric protein complex essential for ex

197 l processes, but the mechanisms by which the exocyst is degraded are unknown.

198 The exocyst is directly involved in regulating soluble N-eth

199 onclude that septin-mediated assembly of the exocyst is necessary for appressorium repolarization and

200 and eyes of zebrafish and mice and that the exocyst is necessary for photoreceptor ciliogenesis and

201 Thus, the exocyst is necessary for, and is likely to direct, the p

202 The vesicle-tethering complex exocyst is one of the crucial cell polarity regulators.

203 The spatio-temporal regulation of the exocyst is only partially understood.

204 We propose that the exocyst is recruited to secretory vesicles by the combin

205 f the complex there, and mistargeting of the exocyst led to secretion defects in cells.

206 expression of Sec4p partially suppressed the exocyst localization defects of mutations in clathrin an

207 prolonged actin disruption led to changes in exocyst localization.

208 Together, our results suggest a model where exocyst mediated vesicle trafficking facilitates branch

209 txA-driven cAMP increase also inhibits Rab11/exocyst-mediated trafficking of host proteins including

210 The apical region of exocyst-mediated vesicle fusion, elucidated by the plasm

211 mics and membrane trafficking, their role in exocyst-mediated vesicle targeting is not very clear.

212 The exocyst mediates the tethering of post-Golgi secretory v

213 pecifically disrupts this interaction led to exocyst mislocalization and a block in exocytosis in viv

214 green fluorescent protein foci in an exo70A1 exocyst mutant.

215 Exocyst mutants displayed altered endocytic and post-Gol

216 Exocyst mutations cause nuclear positioning defects and

217 Loss of either the exocyst or RAL-1 prevents excretory canal lumen extensio

218 expression and stable transfection to induce exocyst overexpression, we show that the exocyst protein

219 We found that exocyst perturbation resulted in resistance to ionizing

220 Here, we report that the exocyst plays a pivotal role in invadopodial activity.

221 Together, our results suggest that the exocyst plays important roles in cell invasion by mediat

222 h the cellular trafficking machinery via the exocyst protein complex.

223 reviously unidentified role for AMPA-R-GRIP1-exocyst protein complexes in activity-dependent AMPA-R t

224 uce exocyst overexpression, we show that the exocyst protein Sec10 regulates primary ciliogenesis.

225 PAR proteins concentrate membrane-localized exocyst proteins to a polarized domain.

226 ate the small GTPase Ral and thereby recruit exocyst proteins to postsynaptic zones.

227 We conclude that Par3 is the long-sought exocyst receptor required for targeted membrane-protein

228 n was seen, arguing against a direct role in exocyst recruitment.

229 ize the function and mechanisms by which the exocyst regulates eye development in zebrafish, we focus

230 c regulation of the evolutionarily conserved exocyst-related processes using mutants in genetically t

231 Thus, Ral regulation of the exocyst represents a control point for postsynaptic plas

232 Furthermore, exocyst Sec8 and polycystin-2 no longer localize to prim

233 The exocyst serves to tether secretory vesicles to cortical

234 r, during infection-related development, the exocyst specifically assembles in the appressorium at th

235 lize each other at endosomes and recruit the exocyst subcomplex containing Sec5.

236 ndings show that P. infestans manipulates an exocyst subunit and thereby potentially disturbs vesicle

237 ding and proteasome-dependent turnover of an exocyst subunit and, thereby, controls exocytosis in fis

238 epeat-containing U-box protein ARC1, and the exocyst subunit Exo70A1 have been proposed to function a

239 One of the exocyst subunit genes, EXO70A1, was previously identifie

240 were used to suppress the expression of each exocyst subunit individually.

241 Both isoforms partly colocalized with the exocyst subunit NtSEC3a at the plasma membrane, possibly

242 Here, we show that a sec3a exocyst subunit null mutant cannot be transmitted throug

243 In zebrafish, depletion of arl13b or the exocyst subunit sec10 causes phenotypes characteristic o

244 at Myo2 interacts directly with Sec4 and the exocyst subunit Sec15.

245 ensitive fission yeast strain mutated in the exocyst subunit Sec3 (sec3-913).

246 previously that the Saccharomyces cerevisiae exocyst subunit Sec6 directly bound the plasma membrane

247 We observe a direct interaction between the exocyst subunit Sec6p and the latter half of the SNARE m

248 yst via a direct interaction with Exo70, the exocyst subunit that guides the polarized targeting of e

249 We focused on the EXO70H4 exocyst subunit, one of the most up-regulated genes in t

250 ic lines to evaluate the requirement of each exocyst subunit.

251 n-based transport mediate the recruitment of exocyst subunits and secretory vesicles during exocytosi

252 In land plants, several exocyst subunits are encoded by double or triple paralog

253 rovide comprehensive evidence that all eight exocyst subunits are necessary in the stigma for the acc

254 Two distinct localization patterns of exocyst subunits at the hyphal tip suggest the dynamic f

255 ce microscopy, we visualized the dynamics of exocyst subunits at this domain.

256 Our study helps to establish the role of the exocyst subunits in tethering and allows the investigati

257 The absent EXO70C2 interactions with core exocyst subunits in the yeast two-hybrid assay, cytoplas

258 Exocyst subunits localize to secretory-active regions of

259 Here we report that the exocyst subunits Sec8, Exo70, and Sec5 bind preferential

260 ng assay in yeast in which each of the eight exocyst subunits was expressed on the surface of mitocho

261 We find that most of the exocyst subunits were able to recruit the other members

262 hypothesized that EXO70A1, along with other exocyst subunits, functions in the Brassicaceae dry stig

263 elucidated by the plasma membrane-associated exocyst subunits, indicates the presence of an exocytoti

264 this study was to examine the requirement of exocyst subunits, which function in docking secretory ve

265 Thus, the exocyst supports DNA repair fidelity by limiting the for

266 the exocyst to primary cilia, whereupon the exocyst targets and docks vesicles carrying ciliary prot

267 t site for plasma-membrane insertion through exocyst-tethered vesicles during cytokinesis.

268 l wall remodeling, likely through control of exocyst tethering and the targeting of other polarity-en

269 They further identify an exocyst tethering complex mediator of outer lateral memb

270 eam effector of Sec4p and a component of the exocyst tethering complex, thus forming a positive-feedb

271 e cell surface through interactions with the exocyst tethering complex.

272 ructures along the cleavage furrow while the exocyst tethers vesicles at the rim of the division plan

273 cruitment of a second tethering complex, the exocyst, that stimulates downstream events of fusion.

274 However, the mechanism by which the exocyst, the exocytosis-specific multisubunit tethering

275 exocyst to the primary cilium, whereupon the exocyst then targets and docks vesicles carrying protein

276 s--Dsl1, conserved oligomeric Golgi, and the exocyst--thought to share a common evolutionary origin.

277 ired for proper membrane localization of the exocyst, thus identifying a molecular link between the b

278 al expressed in Drosophila muscle causes the exocyst to be concentrated in the region surrounding syn

279 osphorylation, resulting from failure of the exocyst to deliver basolateral proteins to the cortex.

280 In accord with the ability of the exocyst to direct delivery of post-Golgi vesicles, const

281 Exo84 by Cdk1-Clb2 during mitosis causes the exocyst to disassemble.

282 t associate with the plasma membrane for the exocyst to function as a vesicle tether.

283 ese results suggest that Cdc42 localizes the exocyst to primary cilia, whereupon the exocyst targets

284 mutations that affect the recruitment of the exocyst to secretory vesicles identified genes encoding

285 edes the nucleotide-dependent arrival of the exocyst to the bladder by a few seconds.

286 AR proteins, we show that RAL-1 recruits the exocyst to the membrane, while PAR proteins concentrate

287 bunit that guides the polarized targeting of exocyst to the plasma membrane.

288 support a model in which Cdc42 localizes the exocyst to the primary cilium, whereupon the exocyst the

289 hown that the highly conserved eight-protein exocyst trafficking complex is required for ciliogenesis

290 The exocyst vesicle-tethering complex functions in polarized

291 h localizes to vesicles and acts through the exocyst vesicle-tethering complex.

292 te 5-kinase (PIPKIgamma) associates with the exocyst via a direct interaction with Exo70, the exocyst

293 embryonic development was impaired when the exocyst was disturbed.

294 rmin) and membrane trafficking (myosin-V and exocyst) were dynamic during cytokinesis.

295 ncogene activation, TBK1 is recruited to the exocyst, where it activates AKT.

296 ila melanogaster to identify the Rab11/Sec15 exocyst, which acts at the last step of endocytic recycl

297 tive ULK1 and Beclin1-VPS34 complexes on the exocyst, which are required for isolation membrane forma

298 rved multisubunit protein complex termed the exocyst, which has been implicated in specific tethering

299 extensively studied tethering complex is the exocyst, which spatially targets vesicles to sites on th

300 owever, no significant colocalization of the exocyst with clathrin was seen, arguing against a direct