ライフサイエンスコーパス: IFT

1 IFT complexes initially accumulate at the base of the ci

2 IFT reduction was identified as the main displacement me

3 IFT relies on molecular motors and IFT complexes that me

4 IFT trains are composed of complexes IFT-A and IFT-B and

5 IFT-B and kinesin are associated to anterograde transpor

6 IFT-based transport of GFP-tubulin is elevated in growin

7 IFT-mediated assembly is length-independent, as train si

8 y conserved mechanism involving more than 20 IFT proteins.

9 also stabilized IFT-B, but failure in IFT-A/IFT-B interaction within the pool at the base of the fla

10 served in these cells: abnormal accumulation IFT complex at the distal tips of the cilia, which assum

11 How input from the cell body affects IFT and ciliary function is not well understood.

12 However, the interaction among IFT motors and IFT complexes during IFT remains elusive.

13 al approaches we show that TTC26/DYF13 is an IFT complex B protein in mammalian cells and Chlamydomon

14 In the IFT140(RNAi) mutant, an IFT-A protein essential for retrograde transport, the IF

15 transport routes for cytosolic proteins: an IFT-dependent path along the axoneme, and a passive-diff

16 T trains are composed of complexes IFT-A and IFT-B and cargo adaptors such as the BBSome.

17 It is required for association of IFT-A and IFT-B at the base of the flagellum and flagellar import

18 movement of two protein complexes (IFT-A and IFT-B) driven by specific kinesin and dynein motors.

19 and multisubunit particles, termed IFT-A and IFT-B, that carry cargo into the cilium.

20 Anterograde trains split apart and IFT complexes mix with each other at the tip to assemble

21 motors were adapted for cilium assembly and IFT function across species.

22 sin-2 motors function in cilium assembly and IFT.

23 ective IFT-A particles enter the axoneme and IFT-B trafficking is severely perturbed.

24 ellar transport protein complexes, IFT-B and IFT-A, which mediate bidirectional protein trafficking a

25 ew, we discuss the role of primary cilia and IFT proteins in the development of bone and cartilage, a

26 ght the current advance of primary cilia and IFT proteins in the pathogenesis of cartilage diseases,

27 GFP-tubulin is elevated in growing cilia and IFT trains carry more tubulin.

28 ein IFT54 interacts with both kinesin-II and IFT dynein and regulates anterograde IFT.

29 for both ciliary heterotrimeric kinesins and IFT particle genes and clarify the function of kif17, th

30 owever, the interaction among IFT motors and IFT complexes during IFT remains elusive.

31 IFT relies on molecular motors and IFT complexes that mediate the contacts with ciliary car

32 dding azide also results in IFT slowdown and IFT components leaving the cilium, but not in activation

33 in binding the IFT motors during anterograde IFT.

34 IF3 and IFT88, and KIF3-mediated anterograde IFT is responsible for photoreceptor transition zone and

35 mbly in response to cessation of anterograde IFT: a slow shortening that is steady over time and a ra

36 in Chlamydomonas induced rapid, anterograde IFT-independent, cytoplasmic microtubule-dependent redis

37 -II and IFT dynein and regulates anterograde IFT.

38 h matches the periodicity of the anterograde IFT-B train.

39 D1bLIC-GFP is transported with anterograde IFT particles to the flagellar tip, dissociates into sma

40 required for the ciliary import of assembled IFT particles at the ciliary base.

41 ail, the intraflagellar transport complex-B (IFT-B), and ciliary kinesin KIF17.

42 of alpha-tubulin utilizes diffusion besides IFT.

43 maintenance, as inhibition of i3A/i3B blocks IFT within 2 min and leads to a complete loss of primary

44 e in the amount of DRC4 cargo transported by IFT particles, and DRC4 transport is downregulated as ci

45 accumulate locally by diffusion and capture; IFT, in contrast, might be required to transport protein

46 n MDCK cells is dominant-negative and causes IFT protein mislocalization and disrupted ciliogenesis.

47 f two mammalian orthologues of Chlamydomonas IFT-A gene, IFT139, namely Thm1 (also known as Ttc21b) a

48 lia, Hedgehog pathway impairment and ciliary IFT accumulations.

49 IFT trains are composed of complexes IFT-A and IFT-B and cargo adaptors such as the BBSome.

50 rectional movement of two protein complexes (IFT-A and IFT-B) driven by specific kinesin and dynein m

51 intraflagellar transport protein complexes, IFT-B and IFT-A, which mediate bidirectional protein tra

52 recognize the length of flagella and control IFT.

53 ns in cytoplasm and suggest that cytoplasmic/IFT dynein heavy chains use a distinct folding pathway.

54 Decreased IFT-A in these short flagella resulted in aggregates of

55 the flagellum and led to severely decreased IFT injection frequency and flagellar-assembly defects.

56 In the absence of CPLANE, defective IFT-A particles enter the axoneme and IFT-B trafficking

57 In a null mutant, lack of IFT74 destabilized IFT-B, leading to flagella assembly failure.

58 e results support the concept that different IFT proteins are responsible for different cargo subsets

59 locomplex, from the large pool of pre-docked IFT-B complexes, and thus initiates ciliary entry of IFT

60 on among IFT motors and IFT complexes during IFT remains elusive.

61 r underpinnings of motor coordination during IFT in vivo.

62 s offer a simple mechanism for how efficient IFT is achieved across diverse organisms despite being c

63 alone is responsible for the atypically fast IFT in C. reinhardtii.

64 During the atypically fast IFT in the green alga C. reinhardtii, on average, 10 kin

65 First, IFT dynein is activated within seconds, redistributing I

66 the KAP subunit fully activating FLA8/10 for IFT in vivo.

67 and further unravel the functional basis for IFT.

68 Mutations in genes coding for IFT components have been associated with a group of dise

69 d primary cilia, a retrograde IFT defect for IFT and BBS proteins, and reduced ciliary entry of membr

70 lution, and we show that it is essential for IFT-B core integrity by mediating interaction between IF

71 triggers a specific mechanism important for IFT regulation that allows the cilium to rapidly adapt t

72 us, ODA16, and outer arm dynein interact for IFT of the latter.

73 Our results yield a model for IFT and cargo trafficking in native mammalian cilia and

74 sitive mutation in the anterograde motor for IFT.

75 ic hedgehog signaling, abnormal staining for IFT-B components, and transcriptomic clustering with cel

76 Unlike dynein-1b, kinesin-II detaches from IFT trains at the tip and diffuses in flagella.

77 suggest that dissociation of kinesin-II from IFT trains serves as a negative feedback mechanism that

78 Thus, we propose that IFT27 separates from IFT-B inside cilia to promote ARL6 activation, BBSome co

79 During ciliary growth, IFT concentrates soluble tubulin in cilia and thereby pr

80 Yet, some ciliated protists do not have IFT components and, like some metazoan spermatozoa, use

81 Instead, higher IFT velocities arise from an increased likelihood that K

82 How IFT trains attain speeds that exceed the unloaded rate o

83 independently of the primary cilium, but how IFT proteins integrate with the cell migration machinery

84 essential for bone development, however, how IFT proteins regulate Hh signalling in osteoblasts (OBs)

85 IFT protein, IFT27, and offer clues into how IFT cargo is selected and transported.

86 m of multiple trains at the ciliary tip, how IFT trains are remodeled in these turnaround zones canno

87 nsion (IFT) studies have shown a decrease in IFT at the O/W interface from approximately 27mN/m to ap

88 oil 1) also stabilized IFT-B, but failure in IFT-A/IFT-B interaction within the pool at the base of t

89 gellar transport (IFT), which is involved in IFT protein recruitment, axonemal engagement of IFT prot

90 wo tubulin subunits, as well as mutations in IFT proteins predicted to disrupt tubulin transport, res

91 etion of ATP by adding azide also results in IFT slowdown and IFT components leaving the cilium, but

92 We demonstrate that actin plays a role in IFT recruitment to basal bodies during flagellar elongat

93 e analysed EVC, EVC2 and Smoothened (SMO) in IFT-A deficient cells.

94 eceptors survive longer compared to those in IFT mutants, which display much weaker basal body mispos

95 However, the functions of individual IFT proteins are mostly unclear.

96 on and function, yet the roles of individual IFT proteins remain unclear.

97 inity comparable with that of the individual IFT subunits.

98 rom disruption of retrograde intraflagellar (IFT) transport of the cilium.

99 This effect is absent in kif3a;IFT double mutants, indicating that IFT proteins have ci

100 dual mechanism and that biochemically links IFT machinery with Hedgehog pathway components.

101 We demonstrated the effect of low IFT at the oil-water interface and wettability alteratio

102 fficking, but our understanding of mammalian IFT is insufficient.

103 nt an architectural model for ODA16-mediated IFT of ODAs.

104 Intriguingly, we found that mobile IFT proteins "switched gears" multiple times from the di

105 grade motor kinesin-II, the retrograde motor IFT dynein, and the IFT-A and -B complexes.

106 Intraflagellar transport (IFT) moves IFT trains carrying cargoes from the cell body into the

107 we reconstituted and purified the nonameric IFT-B core from Chlamydomonas reinhardtii and determined

108 e traffic of IFT dynein with accumulation of IFT complexes near the ciliary tip.

109 terograde traffic of IFT and accumulation of IFT motors and complexes in the proximal region of cilia

110 The amount of IFT injection in dynein mutant cells was higher than tha

111 Recent studies reveal that the amount of IFT injection negatively correlates with the length of f

112 It is required for association of IFT-A and IFT-B at the base of the flagellum and flagell

113 ignalling pathway components, are capable of IFT but with significantly less frequency and/or duratio

114 ike GTPase IFT27/RABL4, a known component of IFT complex B, promotes the exit of BBSome and associate

115 [IFT] 56/DYF13) is an atypical component of IFT-B complex, and deficiency of its highly conserved or

116 oteins (BBSome) as bona fide constituents of IFT in olfactory sensory neurons, and show that they exi

117 actin is perturbed, the normal dependence of IFT recruitment on flagellar length is lost.

118 n in mammalian cells affects the dynamics of IFT particle movement.

119 protein recruitment, axonemal engagement of IFT protein complexes, and so on.

120 ied mechanism that triggers ciliary entry of IFT complexes.

121 t known mechanism directing ciliary entry of IFT complexes.

122 at actin is required for sufficient entry of IFT material into flagella during assembly.

123 the base of the flagellum prevented entry of IFT-A into the flagellum and led to severely decreased I

124 mplexes, and thus initiates ciliary entry of IFT.

125 ase of the flagellum and flagellar import of IFT-A.

126 ely devoid of them, making the importance of IFT to mammalian sperm development unclear.

127 EB1 moved independent of IFT trains, and EB1-FP recovery did not require the IFT

128 The process controlling injections of IFT proteins into the flagellar compartment is, therefor

129 gh resorption, we show that an acute loss of IFT-B through cilia decapitation precedes resorption.

130 e it is challenging to observe the motion of IFT proteins in this crowded region using conventional m

131 at cells regulate the extent of occupancy of IFT trains by tubulin cargoes.

132 tionalize several ciliogenesis phenotypes of IFT mutant strains.

133 nslocation within flagella by the process of IFT.

134 ubs that had accumulated large quantities of IFT particle-like material between the doublet microtubu

135 The recruitment of IFT components to basal bodies is a function of flagella

136 e of D1bLIC in facilitating the recycling of IFT subunits and other proteins, identify new components

137 ts potentially involved in the regulation of IFT, flagellar assembly, and flagellar signaling, and pr

138 ow that, upon disengagement from the rest of IFT-B, IFT27 directly interacts with the nucleotide-free

139 ined that each flagellar pore is the site of IFT accumulation and injection, defining a diffusion bar

140 acking revealed region-dependent slowdown of IFT proteins at the ciliary base, shedding light on stag

141 otors, cannot alone account for the speed of IFT trains in vivo.

142 ere they act to recruit a specific subset of IFT-A proteins.

143 flagella on the basis of the travel time of IFT protein in the flagellar compartment.

144 Here, we report short-trajectory tracking of IFT proteins at the base of mammalian primary cilia by o

145 esulted in diminished anterograde traffic of IFT and accumulation of IFT motors and complexes in the

146 ced ciliary entry and anterograde traffic of IFT dynein with accumulation of IFT complexes near the c

147 likely through dominant negative effects on IFT.

148 pmental Cell illuminate key functions of one IFT protein, IFT27, and offer clues into how IFT cargo i

149 ght on mechanisms underlying Thm1-, Thm2- or IFT-A-mediated ciliopathies.

150 al in dyf13 mutant flagella, unlike in other IFT complex B mutants.

151 ing variants in WDR35, and possibly in other IFT-A components, underlie a number of EvC cases by disr

152 n IFT46, has greatly reduced levels of other IFT-B proteins, and assembles only very short flagella.

153 ter the flagellum and to interact with other IFT-B proteins and its sole expression prevents flagellu

154 Intraflagellar transport proteins (IFT) are required for hedgehog (Hh) signalling transduct

155 address this issue, we focused on a putative IFT protein TTC26/DYF13.

156 is activated within seconds, redistributing IFT components toward the ciliary base; second, the cili

157 t that a length-dependent feedback regulates IFT.

158 The molecular pathways regulating IFT are largely a mystery.

159 spontaneous suppression of ift46-1 restored IFT-B levels and enabled growth of longer flagella, but

160 embly, shortened primary cilia, a retrograde IFT defect for IFT and BBS proteins, and reduced ciliary

161 sight into the role of D1bLIC and retrograde IFT in other organisms.

162 ghly similar to the characterised retrograde IFT phenotype of Dync2h1.

163 t of the evolutionarily conserved retrograde IFT machinery.

164 (IFT), but it does not eliminate retrograde IFT.

165 C that is absolutely required for retrograde IFT and ciliary assembly.

166 odimer and are both essential for retrograde IFT.

167 cilium, but not in activation of retrograde IFT.

168 rather than the ciliary entry or retrograde IFT transport, of various sensory receptors.

169 particles, and begins processive retrograde IFT in <2 s.

170 mpanied by destabilization of the retrograde IFT dynein motor.

171 through cytoplasmic action of the retrograde IFT motor and shedding of ciliary ectosomes.

172 Here, we report that the retrograde IFT motor, cytoplasmic dynein 1b, is required in the cyt

173 cytoplasmic microtubules and the retrograde IFT motor, dynein 1b [14].

174 homodimer is dispensable for distal segment IFT.

175 In complex with several IFT dynein light chains, it is required for correct vert

176 ualized the full range of movement of single IFT trains and motors in Chlamydomonas flagella.

177 6 C-terminus can assemble into and stabilize IFT-B but does not support transport of outer arm dynein

178 conclude that IFT74 is required to stabilize IFT-B; aa 197-641 are sufficient for this function in vi

179 uding part of coiled-coil 1) also stabilized IFT-B, but failure in IFT-A/IFT-B interaction within the

180 ds (aa) of the charged N terminus stabilized IFT-B and promoted slow assembly of nearly full-length f

181 t flagella resulted in aggregates of stalled IFT-B in the flagella.

182 Surprisingly, IFT particle assembly and speed were normal in dyf13 mut

183 The role of the interfacial tension (IFT) and wettability in the microfluidic device was simu

184 d reduced the oil/brine interfacial tension (IFT) from 14.6 to 5.5 mN/m.

185 preciable change in the interfacial tension (IFT) of SSO, indicating that it was not strongly surface

186 Interfacial tension (IFT) studies have shown a decrease in IFT at the O/W int

187 of motors and multisubunit particles, termed IFT-A and IFT-B, that carry cargo into the cilium.

188 developed indirect immunofluorescence test (IFT).

189 We conclude that IFT velocity is governed by (i) the absolute numbers of

190 in kif3a;IFT double mutants, indicating that IFT proteins have ciliary transport-independent roles, w

191 mental Cell, Liang et al. (2014) report that IFT is regulated in part by the phosphorylation status o

192 The IFT machinery is composed of motors and multisubunit par

193 The IFT-B core proteins IFT74 and IFT81 interact directly th

194 Compared with Western blot analysis, the IFT had a 92% sensitivity and a 100% specificity.

195 ure to import both the IFT-A complex and the IFT dynein into the flagellar compartment.

196 The interactions between IFT54 and the IFT motors were also observed in mammalian cells.

197 II, the retrograde motor IFT dynein, and the IFT-A and -B complexes.

198 cate a central role for IFT54 in binding the IFT motors during anterograde IFT.

199 at this is due to failure to import both the IFT-A complex and the IFT dynein into the flagellar comp

200 s mutant, ift46-1, that fails to express the IFT-B protein IFT46, has greatly reduced levels of other

201 Knowledge of how the IFT subunits interact with their cargo is of critical im

202 thereby detected biallelic mutations in the IFT-B-encoding gene IFT172 in 12 families.

203 s with expanded Shh signaling, including the IFT-A complex mutants Ift122 and Ttc21b and embryos expr

204 In the mouse, the IFT proteins are very abundant in testis, but we here sh

205 ssible explanation for the complexity of the IFT machinery.

206 n the gene encoding the IFT88 subunit of the IFT particle.

207 r35(-/-) cilia, but not to the cilium of the IFT retrograde motor mutant Dync2h1(-/-), indicating tha

208 ssed, the higher the overall velocity of the IFT train.

209 ns in the gene IFT81, a key component of the IFT-B complex essential for anterograde transport.

210 TRAF3IP1 encodes IFT54, a subunit of the IFT-B complex required for ciliogenesis.

211 gly, the small GTPase IFT27, a member of the IFT-B complex, turns out to be essential for retrograde

212 To elucidate the architecture of the IFT-B complex, we reconstituted and purified the nonamer

213 roteins SCLT1 and FBF1 and components of the IFT-B complex.

214 order of magnitude greater than that of the IFT.

215 e IFT machinery in a manner dependent on the IFT-A complex.

216 ins, and EB1-FP recovery did not require the IFT pathway.

217 We conclude that the IFT allows sensitive and specific measurement of circula

218 Here, we show that the IFT-B protein IFT54 interacts with both kinesin-II and I

219 nstream of IFT27 to couple the BBSome to the IFT particle for coordinated removal of patched-1 and Sm

220 tein essential for retrograde transport, the IFT dynein components are found at high concentration at

221 osolic proteins tested primarily utilize the IFT path in the anterograde direction, differences are o

222 We propose a model by which the IFT dynein particle is assembled in the cytoplasm, reach

223 all three outer arm heavy chains, while the IFT dynein heavy chain was present in normal amounts.

224 monstrating that CrODA16 associates with the IFT complex with an affinity comparable with that of the

225 se of the flagellum, and associates with the IFT machinery in a manner dependent on the IFT-A complex

226 Thus IFT is essential for the formation but not the maintenan

227 onemes of these neurons show no bias towards IFT kinesin-2 choice, and Kif17 homodimer is dispensable

228 xamine the role of intraflagellar transport (IFT) 20 (Ift20) during polarized migration of epidermal

229 nserved process of intraflagellar transport (IFT) [1, 2].

230 ent of anterograde intraflagellar transport (IFT) [13], but the rapid apical enrichment requires cyto

231 ought to depend on intraflagellar transport (IFT) and diffusion.

232 that assemble via intraflagellar transport (IFT) and function as signaling hubs on eukaryotic cells.

233 Both intraflagellar transport (IFT) and lipidated protein intraflagellar transport (LIF

234 enters cilia as an intraflagellar transport (IFT) cargo and by diffusion.

235 al genes affecting intraflagellar transport (IFT) cause SRPS but they do not account for all cases.

236 codes a subunit of intraflagellar transport (IFT) complex B.

237 genes that encode intraflagellar transport (IFT) components and 74 ciliopathy loci to screen 92 unre

238 ntical, to that of intraflagellar transport (IFT) components.

239 Anterograde intraflagellar transport (IFT) employing kinesin-2 molecular motors has been impli

240 Across eukaryotes, intraflagellar transport (IFT) facilitates cilia biogenesis and cargo trafficking,

241 the first time an intraflagellar transport (IFT) gene is implicated in the pathogenesis of BBS, high

242 impairs retrograde intraflagellar transport (IFT) in humans and the protist Chlamydomonas, accompanie

243 tor for retrograde intraflagellar transport (IFT) in primary cilia.

244 Intraflagellar transport (IFT) is essential for the elongation and maintenance of

245 Anterograde intraflagellar transport (IFT) is mediated by kinesin motor proteins; however, the

246 Intraflagellar transport (IFT) is required for proper function of cilia, although

247 ies and cargoes of intraflagellar transport (IFT) kinesin-2 motors kinesin-II and OSM-3/KIF17 without

248 hout affecting the intraflagellar transport (IFT) kinesin-II.

249 epends on the core intraflagellar transport (IFT) machinery and the associated Bardet-Biedl syndrome

250 The intraflagellar transport (IFT) machinery consists of the anterograde motor kinesin

251 oteins, and on the intraflagellar transport (IFT) machinery.

252 Intraflagellar transport (IFT) motor protein localization, but not velocities, in

253 as an anterograde intraflagellar transport (IFT) motor.

254 Intraflagellar transport (IFT) moves IFT trains carrying cargoes from the cell bod

255 less pronounced in intraflagellar transport (IFT) mutants and reveals that kif3a has a much broader r

256 a are assembled by intraflagellar transport (IFT) of protein complexes that bring tubulin and other p

257 esponsible for the intraflagellar transport (IFT) of tubulin are present in limiting amounts.

258 Moreover, intraflagellar transport (IFT) particle components accumulate in the ciliary shaft

259 cking and entry of intraflagellar transport (IFT) particles, ciliary gating for both membrane and sol

260 two reservoirs of intraflagellar transport (IFT) particles, correlating with phases of ciliary growt

261 Highly conserved intraflagellar transport (IFT) protein complexes direct both the assembly of prima

262 16, as well as the intraflagellar transport (IFT) protein IFT46, but the molecular mechanism by which

263 xpression of known intraflagellar transport (IFT) protein-encoding loci in Atmin mutant embryos.

264 Intraflagellar transport (IFT) proteins are essential for cilia formation and/or f

265 Intraflagellar transport (IFT) proteins are essential for the assembly and bidirec

266 ment and depend on intraflagellar transport (IFT) proteins for their formation and function, yet the

267 do not require the intraflagellar transport (IFT) system for assembly of their flagella.

268 microtubule-based intraflagellar transport (IFT) to organize intercellular signaling.

269 les with polymeric intraflagellar transport (IFT) trains to form a transport machinery that is crucia

270 h sensory cilia by intraflagellar transport (IFT) where KIF3 and KIF17 cooperate to build the axoneme

271 are facilitated by intraflagellar transport (IFT), a bidirectional protein trafficking along the cili

272 by the process of intraflagellar transport (IFT), a highly conserved mechanism involving more than 2

273 flagella requires intraflagellar transport (IFT), a highly regulated kinesin-based transport system

274 bly is mediated by intraflagellar transport (IFT), and cilia defects disrupt hedgehog signaling, caus

275 city of retrograde intraflagellar transport (IFT), but it does not eliminate retrograde IFT.

276 ry out anterograde intraflagellar transport (IFT), ferrying cargo along microtubules (MTs) toward the

277 thin cilia, called intraflagellar transport (IFT), is powered by kinesin-2 and dynein-2 motors.

278 lagella depends on intraflagellar transport (IFT), the bidirectional movement of two protein complexe

279 in the absence of intraflagellar transport (IFT), the predominant protein transport system in flagel

280 al for anterograde intraflagellar transport (IFT), was significantly reduced at (tam)Arl13b(-/-) basa

281 ntinuous cycles of intraflagellar transport (IFT), where ciliary proteins are transported between the

282 and maintained by intraflagellar transport (IFT), whereby the two IFT complexes, IFTA and IFTB, carr

283 of ciliogenesis is intraflagellar transport (IFT), which is involved in IFT protein recruitment, axon

284 rved components of intraflagellar transport (IFT)-mediated assembly and kinesin-13-mediated disassemb

285 t process known as intraflagellar transport (IFT).

286 are assembled via intraflagellar transport (IFT).

287 n a process termed intraflagellar transport (IFT).

288 ein related to the intraflagellar transport (IFT).

289 TTC26 (intraflagellar transport [IFT] 56/DYF13) is an atypical component of IFT-B complex

290 ulations (SLIM) employed an ion funnel trap (IFT) to accumulate ions from a continuous electrospray i

291 raflagellar transport (IFT), whereby the two IFT complexes, IFTA and IFTB, carry cargo via kinesin an

292 , we discuss the various ways eukaryotes use IFT and/or TZ proteins to generate the wide assortment o

293 nts and, like some metazoan spermatozoa, use IFT-independent mechanisms to build axonemes exposed to

294 trograde direction where IFT20 only utilizes IFT, and approximately half of KIF17 and one third of al

295 10 moved at speeds matching those of in vivo IFT [4] but additionally displayed a slow velocity distr

296 associated to anterograde transport whereas IFT-A and dynein participate to retrograde transport.

297 nsight into the interaction of dynein-2 with IFT trains and the origin of diverse functions in the dy

298 ocalised to cilia in puncta, consistent with IFT particles, and physically interacted with WDR34, a m

299 IFT54 directly interacted with IFT dynein subunit D1bLIC, and deletion of residues 261-

300 ow that they exist in 1:1 stoichiometry with IFT particles.