ライフサイエンスコーパス: stalk cell

1 ty mutants - were invaded by the neighboring stalk cell.

2 l cells into leading tip cells and following stalk cells.

3 nteraction behavior exhibited by the tip and stalk cells.

4 EMC is a negative regulator of polar and/or stalk cells.

5 s on to make two cell types: polar cells and stalk cells.

6 tion and concomitant loss of interfollicular stalk cells.

7 lly forms viable spores rather than inviable stalk cells.

8 ae to either refractile spores or vacuolated stalk cells.

9 , rather, some later differentiation step of stalk cells.

10 shion to block signaling to the more distant stalk cells.

11 in concert to form a tip containing only pre-stalk cells.

12 ting bodies arranged about a primary axis of stalk cells.

13 -cell dissociation primarily between tip and stalk cells.

14 t terminal cells belonged to the neighboring stalk cells.

15 uts indicative of defective proliferation of stalk cells.

16 cells, which guide new sprouts, and trailing stalk cells.

17 ess Eya to allow Cas expression in polar and stalk cells.

18 to fruiting bodies of viable spores and dead stalk cells.

19 n of distinct cell behaviors between tip and stalk cells.

20 and by loss of cell contacts between tip and stalk cells.

21 n organization, particularly between tip and stalk cells.

22 trols the cell fate decision between tip and stalk cells.

23 e decision between vascular tip cells versus stalk cells.

24 nfirms Wnt signaling activity in endothelial stalk cells.

25 fruiting bodies with viable spores and dead stalk cells.

26 n differentiation of the swarmer cell into a stalked cell.

27 st as the swarmer cell differentiates into a stalked cell.

28 ision, a motile swarmer cell and an adhesive stalked cell.

29 l with several polar pili and a non-piliated stalked cell.

30 New Z-rings can only form in the replicative stalked cell.

31 mer cell and is localized to the pole of the stalked cell.

32 n-replicating swarmer cell and a replicating stalked cell.

33 but is dispersed throughout the cell in the stalked cell.

34 l types: a motile swarmer cell and a sessile stalked cell.

35 on of the motile swarmer cell to the sessile stalked cell.

36 number of reproductive cycles completed by a stalked cell.

37 armer cell differentiates into a replicative stalked cell.

38 yielding a motile swarmer cell and a sessile stalked cell.

39 for the selective degradation of SsrA RNA in stalked cells.

40 could be classified as either islet cells or stalked cells.

41 rentiation of swarmer cells into replicating stalked cells.

42 rmation; Z-ring formation took place only in stalked cells.

43 urs during the differentiation of swarmer to stalked cells.

44 is present in swarmer cells but absent from stalked cells.

45 uting cells into leading "tip" and trailing "stalk" cells [1, 2].

46 des asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalanc

47 mer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt

48 Of the six vertical (stalked) cells analysed, four were excitatory and, surpr

49 the precursors nor the decision between the stalk cell and polar cell fate but, rather, some later d

50 spore mass that is supported by a column of stalk cells and a basal disk.

51 y role in the germarium for specification of stalk cells and a later role in the vitellarium to patte

52 toward arterial, venous, capillary, and tip/stalk cells and a neural-like identity at full maturatio

53 Later, during budding, stalk cells and additional polar cells are specified in

54 ypes of somatic follicle cells, polar cells, stalk cells and main body epithelial follicle cells, can

55 We therefore propose a model in which stalk cells and polar cells are derived from a precursor

56 Small, restricted clones in stalk cells and polar cells were found adjacent to each

57 simultaneous defects in the specification of stalk cells and polar cells.

58 Eyes absent (Eya) is excluded from polar and stalk cells and represses their fate by inhibiting Cas e

59 rvation to form a fruiting body made of dead stalk cells and reproductive spores, a process that has

60 signaling process controlling maturation of stalk cells and spores and that SDF-1 and/or SDF-2 may b

61 In addition to stalk cells and spores that make up the fruiting bodies

62 ly heterogeneous) fruiting body made of dead stalk cells and spores.

63 very abnormal and no culminant is formed: no stalk cells and very few spores are detected.

64 chimeric fruiting bodies, consisting of dead stalk cells and viable spores.

65 s morphologically distinct daughter cells, a stalked cell and a flagellated swarmer cell.

66 oes asymmetric cell division, resulting in a stalked cell and a motile swarmer cell.

67 division yields dissimilar daughter cells: a stalked cell and a swarmer cell that assembles several p

68 While the holdfast was readily detectable in stalked cells and at the stalked poles of predivisional

69 before the swarmer cells differentiate into stalked cells and the intracellular concentration of Fts

70 g chambers and an absence of interfollicular stalks cells and functional polar follicle cells.

71 rically to produce a vacuolate basal cell, a stalk cell, and a cytoplasmically dense apical cell.

72 a peltate trichome with one basal cell, one stalk cell, and eight glandular (secretory) disc cells.

73 or the complete differentiation of polar and stalk cells, and elevated da levels can even drive the c

74 each ovariole give rise to all polar cells, stalk cells, and main body cells needed to form each fol

75 s reduced in the precursors of the polar and stalk cells, and overexpression of EMC caused dramatic e

76 ein that is normally excluded from polar and stalk cells, and the absence of EYA is sufficient to cau

77 he two differentiated cell types, spores and stalk cells, and their precursors revealed a large numbe

78 in the ultrastructure of the secretory stage stalk cell are also described, as is the ultrastructure

79 Because stalked cells associate tightly with the biofilm through

80 control the maturation of a distinct set of stalk cells at the base of the fruiting body.

81 produces a motile swarmer cell and a sessile stalked cell at each cell division.

82 loss of genes implicated in coordinating tip/stalk cell behaviors, including flt4 and, at later stage

83 inhibition of Alk1 and Alk5, thereby driving stalk-cell behaviour.

84 quires the synthesis of peptidoglycan at the stalk-cell body junction.

85 increase in the diameter of the stalk at the stalk-cell body junction.

86 n which the Ddcdk8- cells differentiate into stalk cells but fail to form spores, indicating a role f

87 ivision in which FtsZ and FtsA are stable in stalked cells but degraded in the non-replicative swarme

88 F-1 biosynthesis, abolished the induction of stalk cells by each of the RhT inhibitors, and this effe

89 appears to be required for the induction of stalk cells by the RhT inhibitors.

90 re induced at the transition from swarmer to stalked cell, coincident with the initiation of DNA repl

91 ferential degradation of CtrA in the nascent stalk cell compartment occurs only after the cytoplasm i

92 ective inactivation of CtrA in the incipient stalked cell compartment.

93 distinct cell types at each cell division: a stalked cell competent for DNA replication, and a swarme

94 After cell division, only the stalked cell contains FtsZ.

95 nt SAM68-dependent functions in both tip and stalk cells contribute to the process of sprouting angio

96 sprouting angiogenesis, endothelial tip and stalk cells coordinately remodel their cell-cell junctio

97 monstrates that disruption of the swarmer-to-stalked-cell developmental sequence does not affect the

98 Spores live and stalk cells die.

99 ferentiation, called PSI-2, and two inducing stalk cell differentiation (DIFs 6 and 7) were resolved.

100 Thus, complete stalk cell differentiation appears to require at least t

101 tself, we propose that RhT inhibitors induce stalk cell differentiation by blocking DIF-1 export, cau

102 Stalk cell differentiation in Dictyostelium has been pro

103 errant behavior in a monolayer assay wherein stalk cell differentiation is induced using the stalk ce

104 r that is normally specific for cells on the stalk cell differentiation pathway, is expressed through

105 -STATa null cells show little or no terminal stalk cell differentiation within the slug.

106 s DIF (a morphogen required for prestalk and stalk cell differentiation).

107 lve extracellular cAMP, a known repressor of stalk cell differentiation, because Dd-STATa null cells

108 protein that in part controls Dictyostelium stalk cell differentiation, is a structural and function

109 The ecmB gene, a general marker for stalk cell differentiation, is greatly overinduced by DI

110 athway that prevents premature commitment to stalk cell differentiation.

111 ecmB gene just as they commit themselves to stalk cell differentiation.

112 pressor protein that regulates commitment to stalk cell differentiation.

113 Conversely activation of the pathway favours stalk cell differentiation.

114 ressed at the slug tip, which is the site of stalk cell differentiation.

115 es c-di-GMP as the morphogen responsible for stalk cell differentiation.

116 -1, the polyketide that induces prestalk and stalk cell differentiation.

117 th its known role as a negative regulator of stalk-cell differentiation.

118 roteolytically turned over during swarmer-to-stalked cell differentiation, coinciding with the loss o

119 is temporally separated from the swarmer-to-stalked cell differentiation, which is normally coincide

120 l division and is degraded during swarmer to stalked cell differentiation.

121 mal Dll4 expression, Notch activity, and tip/stalk cell distribution in the retinal vasculature.

122 In addition, we show that ectopic polar and stalk cells disturb the anterior-posterior polarity of t

123 the preceding stage of the cell cycle (the "stalked" cell), DivL is localized uniformly along the ce

124 thelial cell (EC) specification into tip and stalk cells during angiogenesis.

125 While pslA- cells produce mature, vacuolated stalk cells during multicellular development, pslA- cell

126 role for NRP1 in endothelial tip rather than stalk cells during vessel sprouting.

127 r cell into a sessile, replication-competent stalked cell during its cell cycle.

128 scription factor78 that positively regulates stalk cell elongation by interacting with the polar auxi

129 SYNJ2BP was preferentially expressed in stalk cells, enhanced DLL1 and DLL4 protein stability, a

130 routs revealed that mainly leader cells, not stalk cells, exert contractile forces on the surrounding

131 sions characteristic of tip cells, following stalk cells exhibiting apical-basal polarity, and lumens

132 mechanism of compensatory branching in which stalk cells extend autocellular tubes into neighboring t

133 s required for FSC maintenance and polar and stalk cell fate specification.

134 cess pFC cell differentiation toward a polar/stalk cell fate through suppressing Hedgehog pathway act

135 , if one lineage has a capacity to avoid the stalk cell fate, it may have a selective advantage.

136 ession of Hedgehog can induce both polar and stalk cell fate, presumably by acting on the precursor s

137 ent (EYA), a negative regulator of polar and stalk cell fate.

138 nd the resulting phospho-DivK implements the stalked cell fate.

139 on levels of Jagged destabilizes the tip and stalk cell fates and can give rise to a hybrid tip/stalk

140 PKA and Notch independently regulate tip and stalk cell formation and behavior.

141 development, to varying degrees, and induced stalk cell formation in submerged culture.

142 a polyketide-derived morphogen which drives stalk cell formation in the developmental cycle of Dicty

143 In a monolayer assay of stalk cell formation, the Ax2/gskA- strain is hypersensi

144 gers the maturation of spore cells and those stalk cells forming the stalk.

145 n differentiation of the swarmer cell into a stalked cell, full length PodJ is synthesized and locali

146 As swarmer cells differentiate into stalked cells (G1/S transition), unphosphorylated CpdR a

147 he STAT protein that regulates commitment to stalk cell gene expression, where it is known to functio

148 ascular phenotype, indicated by induction of stalk cell genes.

149 The stalked cell harbours a stalk, a thin cylindrical extens

150 In progeny stalked cells, however, accumulated CcrM that has not be

151 tiate into spores while their victims die as stalk cells in chimeric aggregates.

152 the inducing effects of DIF and readily form stalk cells in monolayer assay, the Dd-STATa null cells

153 NRP1 were coexpressed in endothelial tip and stalk cells in the developing brain.

154 o states: tip cells at the growing front and stalk cells in the vascular plexus behind the front.

155 ivision to yield a motile swarmer cell and a stalked cell in the gram-negative bacterium Caulobacter

156 he Ax2/gskA- strain is hypersensitive to the stalk cell-inducing action of DIF-1 but largely refracto

157 The most effective inhibitor is the stalk cell-inducing chlorinated alkyl phenone, DIF-1.

158 e rank order of pharmacological efficacy for stalk cell induction as they did for Rh123 transport inh

159 Stalked cells initiate a new round of DNA replication im

160 e the ovary, for follicle individualization, stalk cell intercalation, and oocyte localization.

161 o initiate terminal differentiation and form stalk cells is consistent with a model in which Ras func

162 Notch signaling in stalk cells is induced by DLL4 on the tip cells.

163 he morphological change from swarmer cell to stalked cell is a result of changes of function of two b

164 orms, the holdfast structure at the tip of a stalked cell is crucial for mediating the initial attach

165 g late onset blockage near the terminal cell-stalk cell junction and the ectopic extension of autocel

166 A replication until it differentiates into a stalked cell later in the cell cycle.

167 differentiation into a replication-competent stalked cell later in the cell cycle.

168 Notch activation in stalk cells leads to proliferation arrest via an unknown

169 icle cell polarisation, as both follicle and stalk cells localise polarity factors correctly, despite

170 -related activities, including expression of stalk-cell markers and cell proliferation, consistent wi

171 During sprouting, tip cells and ensuing stalk cells migrate collectively into the extracellular

172 lk cell differentiation is induced using the stalk cell morphogen DIF.

173 ow that with differential adhesion only, pre-stalk cells move to the surface of the mound but form no

174 erminal cells being rapidly invaded by their stalk cell neighbor.

175 Apoptosis of stalk cells, normally seen during lens vesicle detachmen

176 es the differentiation between tip cells and stalk cells of neovasculature.

177 en is restricted to differentiated polar and stalk cells once egg chambers form.

178 y after the initiation of DNA replication in stalked cells, one of the origins moves to the opposite

179 concentration and the ratio of nonstalked to stalked cells, over a range of flow rates and found that

180 imental data extends beyond the tip cell vs. stalk cell paradigm, and involves numerous molecular inp

181 pslA- cells exhibit a defect in the prestalk/stalk cell pathways under these experimental conditions.

182 alyses, we find that the regular spatial Tip-Stalk cell patterning can undergo an order-disorder tran

183 at their concentration is low in swarmer and stalked cells, peaks in pre-divisional cells, and then d

184 of neuropilin-1 (Nrp1), which suppresses the stalk-cell phenotype by limiting Smad2/3 activation thro

185 Here we identify instead that the stalk-cell phenotype needs to be actively repressed to a

186 late the acquisition of endothelial tip cell/stalk cell phenotypes, and we showed that modulation of

187 Moreover, DLL4 and DLL1 are expressed in the stalk cell plexus to maintain Notch signaling.

188 hat there was a block in both the swarmer-to-stalked cell polar differentiation program and the initi

189 he carbon starvation block of the swarmer-to-stalked cell polar differentiation program.

190 -distal cell pole and less frequently to the stalked cell pole during the S-phase.

191 We show that PbpC acts at the stalked cell pole to anchor StpX to rigid components of

192 urs at the chromosomal origin located at the stalked cell pole, coincident with the initiation of DNA

193 ted CpdR accumulates and is localized to the stalked cell pole, where it enables ClpXP localization a

194 ation and localization of SpmX to the future stalked cell pole.

195 the developmental regulator SpmX to the old (stalked) cell pole during the G1-->S transition.

196 e regulation of PodJ phase separation by the stalked-cell-pole scaffold protein SpmX is revealed.

197 t scaffold-signaling hubs at the swarmer and stalked cell poles constitutes the basis of ACD.

198 t1 leads to high mTORC1 pathway activity and stalk cell predisposition.

199 While tip and stalk cells previously were thought to be stable and hav

200 ation of new branching vessels; the trailing stalk cells proliferate to develop the vessel.

201 re we show that PTEN is crucial for blocking stalk cell proliferation downstream of Notch, and this i

202 contribution of tip cell migration rate and stalk cell proliferation rate on the formation of new va

203 mediated activities of PTEN are required for stalk cells' proliferative arrest.

204 ctivation to render and maintain endothelial stalk cells quiescent.

205 In contrast, adjacent stalk cells (SCs) trail TCs, generate the trunk of new v

206 rol of available CcrM in progeny swarmer and stalked cells serves to protect the hemimethylated state

207 TA2-AS1 coordinates both metabolism and "tip/stalk" cell signaling to regulate angiogenesis in hypoxi

208 mound stage of Dictyostelium discoideum, pre-stalk cells sort and form a tip at the apex.

209 pressor elements present in the promoters of stalk cell-specific genes.

210 t a distinct spectrin-based mechanism of tip-stalk cell specification during vascular development.

211 rout basements for sprout elongation and tip-stalk cell specification near sprout endpoints, which ma

212 mplying an association of autophagy with tip-stalk cell specification.

213 ls and differentiate to form three ancillary stalk cell structures: the upper cup, the lower cup and

214 stages in the differentiation of one of the stalk cell sub-types.

215 The DNA content of mature stalk cells suggests that they also attain a G1 state pr

216 which many die altruistically as they become stalk cells that support the surviving spores.

217 l types at each cell division: (i) a sessile stalked cell that can initiate DNA replication immediate

218 that represses DNA replication and a sessile stalked cell that replicates its DNA.

219 promotes Wnt/Ctnnb1 signaling in endothelial stalk cells through interactions with Lef1.

220 s and is involved in suppressing neighboring stalk cells to become tip cells during angiogenesis.

221 back loop that specifies endothelial tip and stalk cells to ensure adequate vessel branching and func

222 ss that involves polarized tip cells leading stalk cells to form new capillaries.

223 signaling synergizes with activated Notch in stalk cells to induce expression of the Notch targets HE

224 ng sprouting, beta(IV)-spectrin expresses in stalk cells to inhibit their tip cell potential by enhan

225 eins are essential for the transition from a stalked cell to a predivisional cell.

226 nt flagellar ejection during the swimmer- to stalk-cell transition in the developmental cycle of Caul

227 At the swarmer-to-stalked cell transition and in the stalked compartment o

228 sis as cells enter S-phase at the swarmer-to-stalked cell transition and in the stalked portion of th

229 cleared by proteolysis during the swarmer-to-stalked cell transition as usual, but DNA replication in

230 ation of several dna genes at the swarmer to stalked cell transition occurs in response to cell cycle

231 ne, podJ, is expressed during the swarmer-to-stalked cell transition of the Caulobacter crescentus ce

232 e MmpA for degradation during the swarmer-to-stalked cell transition.

233 ejecting the flagellum during the swarmer to stalked cell transition.

234 th several genes expressed at the swarmer-to-stalked cell transition; while another appears to be con

235 mutants, which are blocked in the swarmer-to-stalked-cell transition and form flagellated, nonmotile

236 po IV genes is induced during the swarmer-to-stalked-cell transition when cells prepare for initiatio

237 Since differentiation into the stalked cell type is irreversible, it is likely that env

238 the origin thus restricts replication to the stalked cell type.

239 es from 13 min in swarmer cells to 55 min in stalked cell types, confirming cell type-specific degrad

240 SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell

241 w that swarmer cells produce more ppGpp than stalked cells upon starvation.

242 e organelle known as the holdfast, which the stalked cell uses to attach to a solid surface.

243 dothelial tip cells with that of endothelial stalk cells using microarray analysis.

244 mybC- cells are able to form both spores and stalk cells very efficiently.

245 No spores or stalk cells were ever made in the mutants, with all cell

246 ne labeled islet cells and only two of seven stalked cells were hyperpolarized by DAMGO.

247 f vascular endothelial growth factor (VEGF), stalk cells, which proliferate and extend the vessels, a

248 Stalked cells, which are actively engaged in DNA replica

249 the proportion was greater than 50% because stalked cells, with their shorter reproductive cycle tim

250 hat aggregated rapidly and formed spores and stalk cells within 14 h of development instead of the no

251 armer cell on a path to differentiate into a stalked cell within a fixed time period.