ライフサイエンスコーパス: midbody

1 ize to the plasma membrane or to the spindle midbody.

2 e accumulation of the exocyst complex at the midbody.

3 evented trafficking of Rab8a vesicles to the midbody.

4 GTPase in the post-mitotic stabilisation of midbody.

5 nserved component of the spindle midzone and midbody.

6 at the centrosome, with none in the spindle midbody.

7 e plasma membrane at the cleavage furrow and midbody.

8 dle poles, centromeres, central spindle, and midbody.

9 SG101 from interacting and localizing to the midbody.

10 and organization of the spindle midzone and midbody.

11 , kinetochores, the mitotic spindle, and the midbody.

12 they remained tethered to each other at the midbody.

13 embrane, kinetochores, spindle poles and the midbody.

14 t much of the ESCRT pathway localizes to the midbody.

15 s localization is separable from that at the midbody.

16 and G(ialpha3) in the centrosomes and at the midbody.

17 terized by the concentration of KIF14 at the midbody.

18 resulting in entrapment of chromatin in the midbody.

19 IP3 and Rab11 localisation to the furrow and midbody.

20 of a pool of cIAP1 that associated with the midbody.

21 ocalizes to mitotic spindle poles and to the midbody.

22 le, and later is concentrated in the spindle midbody.

23 e events, as it localizes to the cytokinetic midbody.

24 ng annexin 11 fail to establish a functional midbody.

25 rce for dissecting the multiple roles of the midbody.

26 neddylation and localization of Cul3 to the midbody.

27 that it is the target of Cul3(KLHL21) at the midbody.

28 , particularly the spindle, centrosomes, and midbody.

29 s exist to recruit ESCRT-III proteins to the midbody.

30 lear pore defects, and tension forces at the midbody.

31 able anchoring of the plasma membrane at the midbody.

32 number of cells where spartin is present at midbodies.

33 sis accompanied by an increase in unresolved midbodies.

34 n and that they localized to centrosomes and midbodies.

35 ar envelopes, centrosomes, kinetochores, and midbodies.

36 the attachment of the plasma membrane to the midbody, a long-postulated function of this organelle.

37 The midbody, a microtubule-rich structure that forms during

38 Plk1 displays little dynamic exchange at the midbody, a process that again is modulated by the kinase

39 es forming the central spindle organizes the midbody, a structure that anchors the ingressed cleavage

40 termed abscission, requires breakage of the midbody, a thin membranous stalk connecting the daughter

41 ed as DNA repair factors, are located at the midbody, a transient structure in the middle of the inte

42 methods to live image furrow ingression and midbody abscission in NSCs within cortical explants.

43 In contrast, quantitative analysis of midbody abscission showed inheritance of the midbody rem

44 m coming back together, and to contribute to midbody abscission.

45 the localization of OGT was decreased at the midbody after Aurora inhibition.

46 inetochore, centrosome, spindle midzone, and midbody, all of which are known to play critical roles i

47 s by blocking syntaxin-2 localization to the midbody, an event essential for completion of cytokinesi

48 otype consistent with destabilization of the midbody and abscission failure.

49 Spartin F24D does not localize to the midbody and acts in a dominant-negative manner to impair

50 for the targeting of apical endosomes to the midbody and apical membrane initiation site (AMIS) durin

51 ansferase (H3K4MT) complexes, resides at the midbody and associates with a subset of midbody regulato

52 egments and the O-P equivalence group of the midbody and caudal segments constitute distinct developm

53 In the 28 midbody and caudal segments, however, there are two init

54 x and maintaining an association between the midbody and cell cortex.

55 ons regulate its movement from centrosome to midbody and completion of abscission.

56 machinery mediating AMIS recruitment to the midbody and determined that both branched actin and micr

57 nsport (ESCRT) proteins are recruited to the midbody and direct the severing of the intercellular bri

58 e that individual vesicles accumulate at the midbody and generate a reserve vesicle pool that is dist

59 ts occurs without Cep55 and ESCRT-III at the midbody and is not affected by ESCRT depletion.

60 Second, the midbody and midbody ring are released into a specific da

61 nce Plk1 is degraded can Cep55 target to the midbody and promote abscission.

62 This EB3 phosphorylation was enriched at the midbody and shown to control cortical microtubule growth

63 ion is usually observed on both sides of the midbody and takes 65 to 75 min to complete.

64 mportant for the recruitment of MITD1 to the midbody and that MITD1 participates in the abscission ph

65 is important for spartin recruitment to the midbody and that spartin participates in cytokinesis.

66 tion leads to elevated levels of Plk1 at the midbody and the failure of Cep55 recruitment.

67 Arf6 is localised to the furrow and midbody and we show that Arf6-GTP functions to localise

68 either of these complexes is targeted to the midbody and whether their delivery is coordinated.

69 in centrosomes, mitotic spindles, midzones, midbodies, and cilia are all supportive of roles in micr

70 Smurf2 localizes to the centrosome, mitotic midbody, and centromeres.

71 Spartin colocalizes with Ist1 at the midbody, and depletion of Ist1 in cells by small interfe

72 alizes to the centrosomes, kinetochores, the midbody, and nuclear envelopes during the cell cycle.

73 at the tips of cortical microtubules and the midbody, and perturbation of GEF-H1 function induced mit

74 rosomes, interkinetochore/centromere region, midbody, and pseudocleavage furrows without DNA damage a

75 ocalize to centrosomes, mitotic spindles and midbody, and selective inhibition or silencing of TBK1 t

76 tokinesis, loss of Polo-like kinase-1 at the midbody, and the accumulation of binucleate cells.

77 tein ELKS and Rab8A-positive vesicles to the midbody, and the depletion of ELKS and Rab8A also leads

78 Electron-dense material and midbodies are both absent from the elongated midzones, a

79 Deriving from midzones, midbodies are organized by a set of microtubule interact

80 structural and regulatory components of the midbody are either absent or mislocalized.

81 ar region and subsequently trafficked to the midbody area during later stages of cytokinesis.

82 nt with Rab14's reported localization to the midbody as well as its effects upon Cdc42.

83 l for both the formation and function of the midbody, assembles in a sharp band at the centre of the

84 Despite its importance, understanding of midbody assembly and its regulation is still limited.

85 s represent the most detailed description of midbody assembly and maturation to date and may help elu

86 KIF20B is not required for midbody assembly, but may accelerate or coordinate midbo

87 of Plk1, a key regulator of cytokinesis, in midbody assembly.

88 , an actin disassembly factor, in organizing midbody-associated protein complexes.

89 ends, as well as mislocalization of several midbody-associated proteins.

90 We propose that MICAL3 acts as a midbody-associated scaffold for vesicle targeting, which

91 It was additionally observed in the midbody at cytokinesis.

92 crotubule-rich intercellular bridge with the midbody at its centre.

93 e is concentrated at the mitotic spindle and midbody at M phase.

94 romeres in metaphase and translocated to the midbody at telophase.

95 ingressing from basal to apical, forming the midbody at the apical membrane.

96 PRK2 is required for abscission of the midbody at the end of the cell division cycle and for ph

97 t of the cell cycle but then migrates to the midbody at the start of cytokinesis, suggesting that the

98 s the relatively new field of postabscission midbody biology, particularly focusing on how it may act

99 At the midbody, BRCA2 influences the recruitment of endosomal s

100 spartin does not affect Ist1 localization to midbodies but markedly impairs cytokinesis.

101 b localizes predominately to centrosomes and midbodies, but also to spindle microtubules and transien

102 nits (CHMP4B and CHMP2A/B) accumulate to the midbody, but they are highly disorganized, failing to fo

103 scribe how the structural composition of the midbody changes during progression throughout cytokinesi

104 Centralspindlin kinesin-6/RhoGAP complex, a midbody component critical for both the formation and fu

105 ion of the nonmuscle myosin II NMY-2 and the midbody component CYK-7 at the bridge, in part by limiti

106 nd cytoplasmic organelles but exclude normal midbody components such as MKLP1 and Aurora B.

107 leavage furrow (anaphase and telophase), and midbody (cytokinesis) during cell division in immortaliz

108 Recruitment of WDR5 to the midbody dark zone appears to require integrity of the WD

109 Functional dissection of the midbody demonstrated the importance of lipid rafts and v

110 The midbody directs the final membrane abscission reaction a

111 eir maintenance or proliferation and then at midbodies during abscission, thereby helping ensure the

112 at spindle poles during mitosis and then at midbodies during cytokinesis, implying that these protei

113 and bidirectional growth of microtubules in midbodies during cytokinesis.

114 6-GTP functions to localise FIP3 and FIP4 to midbodies during cytokinesis.

115 metaphase and to the spindle midzone and the midbody during anaphase and cytokinesis.

116 4 and PRC1 colocalize on the spindle midzone/midbody during anaphase and cytokinesis.

117 or the first time, they were detected at the midbody during cell division.

118 led-coil protein centriolin localized to the midbody during cytokinesis and was required for abscissi

119 CRT-associated protein-were recruited to the midbody during cytokinesis by interaction with centrosom

120 arase localizes to the ingressing furrow and midbody during cytokinesis in the C. elegans embryo.

121 ome in interphase cells and recruited to the midbody during cytokinesis, is a regulator required for

122 nteraction mediates MITD1 recruitment to the midbody during cytokinesis.

123 cell junctions and in mitotic cells, at the midbody during cytokinesis.

124 oles from interphase to telophase and at the midbody during cytokinesis.

125 phase and concentrate on the central spindle/midbody during cytokinesis.

126 lizes with MyoGEF at the central spindle and midbody during cytokinesis.

127 some targeting and AMIS formation around the midbody during epithelial lumenogenesis.

128 n interphase cells, which relocalizes to the midbody during late phases of mitosis.

129 o the spindle midzone in anaphase and to the midbody during normal cytokinesis.

130 OGT colocalized to the midbody during telophase with Aurora B.

131 alizes to microtubules in interphase and the midbody during telophase, and its protein levels decreas

132 cate a novel mechanism for the regulation of midbody dynamics in which ARF6 protects the compacted ce

133 r (which induces a P-to-O fate change in the midbody) fails to affect O/P patterning in the rostral r

134 pindle structures, reduction of K-fibers and midbody fibers, disrupted chromosome movement, and atten

135 increases localization of active RHOA at the midbody, followed by diffusion to the flanking zones.

136 wo new tricellular tight junctions flank the midbody following cytokinesis.

137 the appropriate level of active RHOA at the midbody for faithful completion of cytokinesis and genom

138 e furrow, and both proteins are required for midbody formation and proper localization of Pavarotti a

139 ndle during anaphase is essential for proper midbody formation and the segregation of daughter cells

140 diomyocytes after apical resection exhibited midbody formation consistent with abscission failure.

141 cytokinesis from embryonic hearts exhibited midbody formation consistent with successful abscission,

142 light chain and localized at the site of the midbody formation in dividing wild-type erythroblasts.

143 motility along microtubules in vitro and for midbody formation in vivo.

144 Finally, we show that CIT-K's role in midbody formation is conserved in human cells.

145 hat both motor and stalk domains function in midbody formation, whereas the tail is essential for com

146 lays both structural and regulatory roles in midbody formation.

147 hat CIT-K is likely to act at the top of the midbody-formation hierarchy by connecting and regulating

148 3-3 for binding to centralspindlin such that midbodies formed by centralspindlin mutants that can bin

149 ein 14 (Tex14), which has been implicated in midbody function, is recruited to KTs by Plk1 in a Cdk1-

150 h receptors with axons in posterior roots of midbody ganglia.

151 each daughter, the smaller cluster near the midbody gradually migrates to rejoin the major cluster o

152 Recently, the midbody has gained prominence for exerting postmitotic f

153 (which induces an O-to-P fate change in the midbody) has no effect in the rostral region.

154 g (which effects a P-to-O fate change in the midbody) has no effect on the patterning of O and P fate

155 Although several essential components of the midbody have recently been identified, essential compone

156 ed on chromatin bridges and near the midzone/midbody in an AIR-2-dependent manner.

157 lin ring complex of early mitosis and to the midbody in late cytokinesis by immunofluorescence assay

158 Annexin 11 is recruited to the midbody in late telophase, where it forms part of the de

159 may be related to the specialization of the midbody in neural cells.

160 In this review, we detail the role of the midbody in orchestrating abscission, as well as discuss

161 d localization of both KIF14 and CRIK at the midbody in patient-derived fibroblasts.

162 tase B2 (MsrB2) is strongly recruited at the midbody in response to the presence of lagging chromatin

163 n abscission, as it fails to localize to the midbody in SCCRO-deficient cells during abscission, and

164 metaphase, while it was concentrated at the midbody in telophase in meiotic oocytes.

165 st that WDR5 is specifically targeted to the midbody in the absence of chromatin and that it promotes

166 red somatic cells, TEX14 can localize to the midbody in the absence of other germ cell-specific facto

167 y divisions, furrow ingression asymmetry and midbody inheritance is consistent, suggesting specific r

168 The midbody is a transient structure that connects two daugh

169 The midbody is an organelle assembled at the intercellular b

170 ion and the conclusion of cell division, the midbody is either released or rapidly degraded by one of

171 t, we find that the targeting of FIP3 to the midbody is independent of Rab11.

172 We show that after cytokinesis, the midbody is inherited by one of the daughter cells as a r

173 ork has shown that targeted secretion to the midbody is required to complete cell division.

174 elch protein KLHDC8B, which localizes to the midbody, is expressed during mitosis, and is mutated in

175 s (rostrum body, anterior midbody, posterior midbody, isthmus, and splenium) and for overall CC size,

176 ns had greater connectivity in the posterior midbody/isthmus of the corpus callosum and that fraction

177 ensable for the formation of the midzone and midbody, it promotes contractility and is required for t

178 elective, as other nonmembranous organelles (midbody, kinetochore) and membrane-bounded organelles (m

179 MLL1 binding to this pocket also abolish the midbody localization of WDR5.

180 il play distinctive roles in stabilizing the midbody matrix and maintaining an association between th

181 exogenous CHO1 restored the formation of the midbody matrix and rescued cytokinesis in siRNA-treated

182 tial for completion of cytokinesis after the midbody matrix has formed.

183 nucleate cells because of the absence of the midbody matrix in the middle of the intercellular bridge

184 ating protein (MgcRacGAP) and converts these midbody matrix proteins into stable intercellular bridge

185 ules during anaphase, and assembles into the midbody matrix surrounding the compacted midzone microtu

186 the midzone and prevents the formation of a midbody matrix.

187 In addition, the NSC midbody maturation defects are not rescued by p53 deleti

188 y assembly, but may accelerate or coordinate midbody maturation.

189 hought to be a remnant of cell division, the midbody (MB) has recently been shown to have roles beyon

190 ission, because it recruits ESCRT-III to the midbody (MB), the site of abscission.

191 dy stage suggests the possibility of a novel midbody-mediated pathway for p53 activation.

192 The midbody mediates abscission by recruiting many factors,

193 cally regulate the localization of lipids to midbodies, membrane-based structures where cleavage occu

194 , apparently because the spindle midzone and midbody microtublues were absent during late mitosis.

195 ingression and abscission, during which the midbody microtubule bundle provides both structural supp

196 promotes abscission, perhaps by facilitating midbody microtubule disassembly.

197 Additionally, EB3 promoted midbody microtubule stability and, consequently, midbody

198 ily member, and cIAP1 were both localized on midbody microtubules at telophase, and also interacted w

199 ies of KIF14 are well suited for stabilizing midbody microtubules during cytokinesis.

200 Consistent with these defects, midbody microtubules in WDR5 knockdown cells also displa

201 ociation between the plasma membrane and the midbody microtubules prior to abscission.

202 ing-derived midbody ring, it is assumed that midbody microtubules scaffold the abscission machinery.

203 In this paper, we assess the contribution of midbody microtubules versus the midbody ring in the Caen

204 Surprisingly, midbody microtubules were dispensable for both stages.

205 entral role of the midbody ring, rather than midbody microtubules, in their execution.

206 illomavirus E2 colocalizes with MKlp2 in the midbody/midplate during late mitosis.

207 alterations to cytokinesis, including apical midbody migration in polarizing epithelial cells of the

208 SSRP1 colocalizes with the spindle and midbody MTs, and associates with MTs both in vitro and i

209 s produced by the rostral OP pathway and the midbody O and P pathways are very similar.

210 at centrosomes and are then recruited to the midbodies of dividing cells through direct interactions

211 IST1, CHMP1, and VPS4 were recruited to the midbodies of dividing cells, and depleting either IST1 o

212 entrosomal compartment and especially in the midbody of dividing cells.

213 in that localizes to the cleavage furrow and midbody of mitotic cells, where it is required for the c

214 c I-2 localized to the spindle, midzone, and midbody of mitotic human epithelial ARPE-19 cells.

215 Recruitment of ESCRT-I/II complexes to the midbody of telophase cells initiates ESCRT-III assembly

216 ired for cytokinesis and is localized on the midbody of the contractile ring.

217 from the inside out by the microtubule-based midbody or from the outside in by the contractile ring-d

218 Thus, Kif20b is required for proper midbody organization and abscission in polarized cortica

219 0b is involved in cerebral cortex growth and midbody organization of neural stem cells.

220 ter capillary area in the pes (p = .002) and midbody (p = .021).

221 n groups in whole hippocampus (p = .013) and midbody (p = .036).

222 in the anterior (pes, p = .042) and central (midbody, p = .004) DG, and greater capillary area in the

223 and mark the center of the cell in lieu of a midbody/phragmoplast.

224 cal domain, mitotic spindle orientation, and midbody position, consistent with Rab14's reported local

225 ibution of pPLK4 midzone/cleavage furrow and midbody positions pPLK4 to play a functional role in cyt

226 r several CC regions (rostrum body, anterior midbody, posterior midbody, isthmus, and splenium) and f

227 trosome protein 55 (Cep55), a centrosome and midbody protein essential for abscission.

228 report the characterization of the intricate midbody protein-protein interaction network (interactome

229 ic and microtubule disassembly at a specific midbody region called the secondary ingression.

230 to dorsal and then centripetally toward the midbody region on the dorsal basement membrane.

231 DTCs continue their migration away from the midbody region.

232 lineages in the segments of the rostral and midbody regions.

233 the midbody and associates with a subset of midbody regulatory proteins, including PRC1 and CYK4/MKL

234 division factors to the spindle midzone and midbody remain unclear.

235 midbody abscission showed inheritance of the midbody remnant by one daughter cell, indicating that cy

236 After NSC divisions in vitro, midbody remnants are more often retained on the daughter

237 Postabscission midbody remnants are observed at the apical membranes of

238 Tethered midbody remnants dancing across apical microvilli, encou

239 est that regulation of abscission timing and midbody remnants in embryonic NSCs may influence proper

240 indle, and in most cases, dissolution of the midbody, reopening of the cleavage furrow, and realignme

241 In contrast, the contractile ring and midbody required for cytokinesis, the final stage of mit

242 otect against genetic damage by coordinating midbody resolution with the abscission checkpoint.

243 cytokinesis resolves with abscission of the midbody, resulting in independent daughter cells, germ c

244 in that only one daughter cell inherits the midbody ring (MR) upon completion of abscission even in

245 e ring (CR) is coupled to the formation of a midbody ring (MR), through poorly understood mechanisms.

246 nputs into Sticky recruitment to the nascent midbody ring and show that each input is subsequently re

247 Second, the midbody and midbody ring are released into a specific daughter cell

248 The vesicles move to the midbody ring asymmetrically from one prospective daughte

249 Collectively, these results show how midbody ring biogenesis depends on the coordinated actio

250 n through this stage required the septins (a midbody ring component) but not the membrane-remodeling

251 ch of these tissues after internalization of midbody ring components.

252 nase is one important component required for midbody ring formation but its mechanisms of action and

253 nd Anillin, a key scaffold also required for midbody ring formation.

254 tribution of midbody microtubules versus the midbody ring in the Caenorhabditis elegans embryo.

255 embrane scission occurs on both sides of the midbody ring with random order and that completion of th

256 e outside in by the contractile ring-derived midbody ring, it is assumed that midbody microtubules sc

257 ission and highlight the central role of the midbody ring, rather than midbody microtubules, in their

258 ion at, and for the integrity of, the mature midbody ring.

259 hey promote subsequent formation of a stable midbody ring.

260 lation of v-SNARE-containing vesicles at the midbody ring.

261 n, and septins and in forming the subsequent midbody ring.

262 uire centriolin for localization to a unique midbody-ring structure, and disruption of either complex

263 tors associated with longitudinal muscles in midbody segments of medicinal leeches, only the ventral

264 tion differ substantially in the rostral and midbody segments, even though the set of differentiated

265 However, apical midbodies show changes in number, shape and positioning

266 ody microtubule stability and, consequently, midbody stabilization necessary for efficient cytokinesi

267 ith addition of an Aurora B inhibitor at the midbody stage suggests that Aurora B is the target of SC

268 tion of p53 in the nucleus of mutant NSCs at midbody stage suggests the possibility of a novel midbod

269 is also sufficient to increase the number of midbody-stage cells and, likewise, triggers distinctive

270 We further find that ATR activity in midbody-stage cells links postmitotic genome surveillanc

271 the pore basket components Tpr and Nup 50 in midbody-stage cells.

272 ge of cytokinesis, Cep55 is required for the midbody structure and for the completion of cytokinesis.

273 specific role for BRCA2 in the regulation of midbody structure and function, separate from DNA damage

274 ndlin to Cep55, which, in turn, controls the midbody structure and membrane fusion at the terminal st

275 ed during mitosis, where it localizes to the midbody structure connecting cells about to separate dur

276 It is currently unclear how the midbody structure is stably maintained during this perio

277 olymerization at the edge of the cytokinetic midbody structure, located at the center of the intercel

278 of cardiomyocytes accompanied by unresolved midbody structures.

279 positive vesicles at the cleavage furrow and midbody that is not a consequence of chromosome nondisju

280 ere we show that BRCA2 is a component of the midbody that is recruited through an interaction with Fi

281 and the ESCRT-associated protein ALIX to the midbody (the structure that tethers two daughter cells)

282 nts, the various observed transitions of the midbody, the beginning of ciliogenesis, and the accumula

283 s the three microtubule-based organelles-the midbody, the centrosome, and the cilium-in the same cell

284 ps that relocalize to different parts of the midbody: the bulge, the dark zone, and the flanking zone

285 is recruited to the central spindle and the midbody through a direct interaction with the centralspi

286 thway, ALIX and TSG101, are recruited to the midbody through direct interactions with the phosphoprot

287 s to microtubules of the central spindle and midbody throughout cytokinesis, at sites distinct from t

288 microtubule motor protein, localizes at the midbody to finalize cytokinesis by interacting with CRIK

289 along the intercellular bridge away from the midbody until it reaches an equilibrium position, determ

290 ination-promoted turnover of Aurora B at the midbody was deficient in SCCRO- and KLHL21-deficient cel

291 ures, such as centrosomes, kinetochores, and midbody, we propose that the observed feed-forward mecha

292 Midbodies were isolated from mammalian cells, proteins w

293 the centrosomes, the spindle poles, and the midbody when ectopically expressed in HeLa and U2OS cell

294 m recycling endosomes to the cleavage furrow/midbody where they are tethered prior to fusion events v

295 ed to presumptive abscission sites in mature midbodies, where they may regulate the endosomal sorting

296 During cytokinesis, LARG is condensed in the midbody, where it colocalizes with RhoA.

297 d apoptosis and defects in maturation of NSC midbodies, which mediate cytokinetic abscission.

298 nimal cells requires the central spindle and midbody, which contain prominent microtubule bundles.

299 atic cells concludes with the formation of a midbody, which is abscised to form individual daughter c

300 of both the spindle within the cell and the midbody within the mitotic spindle, with differential re