ライフサイエンスコーパス: neuroblast

1 bpopulation of Drosophila neural stem cells (neuroblasts).

2 y asymmetrically dividing neural stem cells (neuroblasts).

3 eurons born post-embryonically from the same neuroblast.

4 ation, we used cultures of chick sympathetic neuroblasts.

5 maintained proliferation of MYCN/ALK(F1174L) neuroblasts.

6 1) is required to generate INPs from type II neuroblasts.

7 selectively enriched or repressed in certain neuroblasts.

8 c mechanism controlling delamination of otic neuroblasts.

9 ducts were present in adjacent late IPCs and neuroblasts.

10 n-canonical Wnt signaling in differentiating neuroblasts.

11 f lagging acentric chromosomes in Drosophila neuroblasts.

12 rolled progenitor supply and maturation into neuroblasts.

13 ype, which is typical of immature, migrating neuroblasts.

14 , is observed in proliferating noradrenergic neuroblasts.

15 morphological maturation of differentiating neuroblasts.

16 Discs Large apical localization in metaphase neuroblasts.

17 tence to generate INPs in trx mutant type II neuroblasts.

18 agments generated in Drosophila melanogaster neuroblasts.

19 to suppress the formation of ectopic type II neuroblasts.

20 dedifferentiation of INPs back into type II neuroblasts.

21 cells including transit-amplifying cells and neuroblasts.

22 ntrioles in cultured S2 cells and Drosophila neuroblasts.

23 rom these lips was performed with markers of neuroblasts.

24 ression of fzy suppresses the death of these neuroblasts.

25 that prevents dedifferentiation of INPs into neuroblasts.

26 p/Lin-28+ neuroblasts transition to Syncrip+ neuroblasts.

27 spindle orientation in delaminated embryonic neuroblasts.

28 enhancer in an inactive but poised state in neuroblasts.

29 sibling neurons of single progenitors called neuroblasts.

30 uring asymmetric cell division of Drosophila neuroblasts.

31 Pax-6 orthologue, expressed in mushroom body neuroblasts.

32 rodents, it is mainly composed of chains of neuroblasts.

33 om constitutive Notch activity in Drosophila neuroblasts.

34 gene castor sub-divides its large window in neuroblast 5-6 by simultaneously activating two cell fat

35 entricle had the morphology of very immature neuroblasts, a round shape with no processes, whereas th

36 apoptosis occurred in differentiating (Dcx) neuroblasts, accompanied by reduced newborn neuron survi

37 Loss of orthodenticle from this neuroblast affects molecular properties, neuroanatomical

38 dense plexus of capillaries, with which only neuroblasts, among the entire population of progenitors,

39 inates from the excretory system to become a neuroblast and is replaced by the G2 cell.

40 o the accumulation of actively proliferating neuroblasts and a lethal brain tumor phenotype.

41 red for compact, directional organization of neuroblasts and astrocytes within the pathway and effici

42 partners are expressed by subpopulations of neuroblasts and astrocytes within the SVZ/RMS/OB system

43 ed by ephrins expressed by subpopulations of neuroblasts and astrocytes, is required for compact, dir

44 EphA4 kinase activity resulted in misaligned neuroblasts and disorganized astrocytes in the RMS/SVZ,

45 aRIII, GPC1, GPC3, SDC3, and SDC4, is low in neuroblasts and high in the Schwannian stroma.

46 is ablated in both KIF1Bbeta-deficient mouse neuroblasts and human neuroblastomas that lack KIF1Bbeta

47 Embryonic type II neuroblasts and INPs undergo quiescence, and produce emb

48 lastoma is characterized by undifferentiated neuroblasts and low schwannian stroma content.

49 ting in dramatic neoplastic proliferation of neuroblasts and massive larval brain overgrowth.

50 ntrol dynamic interactions between migratory neuroblasts and surrounding astrocytes are of particular

51 ue involves immortalizing GAL4 expression in neuroblasts and their descendants.

52 We developed new genetic tools that target neuroblasts and their diverse descendants, increasing ou

53 able to readily distinguish the delaminating neuroblasts and to describe progressive states of gene e

54 tumor suppressor in both neural stem cells (neuroblasts) and epithelia.

55 due to expansion of proliferating embryonic neuroblasts, and Let-7-independent functions are implica

56 lls in 1 tumor and was also discovered among neuroblast-appearing cells in another.

57 Neurons from a neuroblast are often so diverse that many neuron types r

58 number and the cell fates generated by each neuroblast are very precisely controlled in a cell auton

59 Subventricular zone neuroblasts are aligned in tightly bundled chains within

60 Drosophila neuroblasts are an excellent model for investigating how

61 Drosophila neural stem cells (neuroblasts) are a powerful model system for investigati

62 Neuroblasts arising post-IR derive from activated qNSCs

63 y generated rodent subventricular zone (SVZ) neuroblasts as they transit along the lateral ventricles

64 l mesencephalic tissue, rich in dopaminergic neuroblasts, as restorative treatment for their Parkinso

65 ot alter the number of doublecortin-positive neuroblasts at the end of the treatment period.

66 oral fate by RNA-sequencing lineage-specific neuroblasts at various developmental times.

67 a paracrine signal, contributes to maintain neuroblasts attached to each other while they migrate in

68 izes asymmetrically to mother centrosomes in neuroblasts, both requiring Bld10, a basal body protein

69 effect on transit-amplifying progenitors or neuroblasts but was restricted to neural stem cells.

70 al progenitors (transit amplifying cells and neuroblasts) but not NSCs (quiescent and activated) unde

71 be converted to doublecortin (DCX)-positive neuroblasts by a single transcription factor, SOX2, in t

72 trophic cellular stress and p53 to eliminate neuroblasts by necrosis.

73 Fruit fly neuroblasts can either self-renew, rest or take on a spe

74 Importantly, these induced neuroblasts can mature into synapse-forming neurons in v

75 Neuroblasts carrying the novel fzy allele or exhibiting

76 ration of spatial inputs by a fixed temporal neuroblast cascade thus acts as a powerful mechanism for

77 Once in the OB, neuroblasts cease to express S1P1, which results in cell

78 e gyrus, with higher expression intensity in neuroblast cells as compared to quiescent stem cells and

79 Cell proliferation and neuroblast chain formation in subventricular zone (SVZ)

80 of mushroom body, antennal lobe and type II neuroblasts compared with non-selective neuroblasts, neu

81 e (Rok) enriches for activated Myosin on the neuroblast cortex prior to nuclear envelope breakdown (N

82 s establish a Myosin gradient at the lateral neuroblast cortex, necessary to trigger an apically dire

83 Rok and Protein Kinase N (Pkn) on the apical neuroblast cortex.

84 and neurogenic genes, resulting in increased neuroblast death and functionally aberrant newborn neuro

85 Lin28 knockdown in cultured sympathetic neuroblasts decreases proliferation, whereas Let-7 inhib

86 mental patterning genes such as intermediate neuroblasts defective (ind).

87 eling of the neuronal progenitor domain upon neuroblast delamination, and reveals that the order and

88 ion, and reveals that the order and place of neuroblasts' delamination from the otic epithelium prefi

89 nematode C. elegans, the migration of the QR neuroblast descendants requires multiple Wnt ligands and

90 show that spindle polarity is maintained in neuroblasts despite centrosome detachment, with the pole

91 erent signaling pathways active during early neuroblast development and prosensory domain specificati

92 of central projections, and (2) delaminated neuroblasts differentiate in close contact with the neur

93 Y5Y), soluble HBEGF is sufficient to promote neuroblast differentiation and decrease proliferation.

94 stoma cell lines with soluble HSPGs promoted neuroblast differentiation via FGFR1 and ERK phosphoryla

95 sed its association with the adapter protein neuroblast differentiation-associated protein (AHNAK, de

96 th by releasing soluble factors that promote neuroblast differentiation.

97 Proliferating MYCN/ALK(F1174L) neuroblasts display a differentiated phenotype but diffe

98 We found that Ensconsin/MAP7 mutant neuroblasts display shorter metaphase spindles, a defect

99 ctopically expressed, some non-mushroom body neuroblasts divide independent of dietary nutrient condi

100 mmetry in the daughter cell sizes of the Q.a neuroblast division but by a mechanism that is independe

101 eads to randomly inherited centrosomes after neuroblast division.

102 Neuroblast divisions in the nematode Caenorhabditis eleg

103 entified genes that, when mutated, result in neuroblast divisions that generate daughter cells that a

104 In humans, it is organized in layers where neuroblasts do not form chains.

105 out neurogenesis by activating a conditional neuroblast driver in specific lineages using various int

106 s on loss of the GAL4 repressor, GAL80, from neuroblasts during early neurogenesis.

107 which are generated by neural stem cell-like neuroblasts during embryonic and postembryonic developme

108 rostral migratory stream, a pathway used by neuroblasts during their transit toward olfactory bulb l

109 ains the proliferation of neural stem cells (neuroblasts) during starvation.

110 gaster nervous system development, revealing neuroblast dynamics throughout an entire embryo.

111 The analysis of the neuroblast ectopic migration from the SVZ toward the les

112 of Lin28B in embryonic mouse sympathoadrenal neuroblasts elicits postnatal NB formation.

113 We find that most neuroblasts enter and exit cell cycle in a nutrient-depe

114 In this study, we show that when neuroblasts enter quiescence, the differentiation factor

115 In mice lacking TSHZ1, neuroblasts exhibited a normal tangential migration to t

116 When Eyeless is knocked down, mushroom body neuroblasts exit cell cycle when nutrients are withdrawn

117 Neuroblasts experiencing catastrophic cellular stress, o

118 ophila embryonic nervous system development, neuroblasts express a programmed cascade of five tempora

119 EGFR(+) oligodendrocyte progenitors, but not neuroblasts, express high levels of a T3-inactivating de

120 inmo/Imp and activate Syncrip, plus two late neuroblast factors, Broad and E93.

121 thin the radial dimension, and many immature neuroblasts failed to exit the rostral migratory stream.

122 tic progenitors activate NEUROG1 and adopt a neuroblast fate is incompletely understood.

123 Notch is required in type II neuroblasts for normal development of their transit ampl

124 ges, we marked and isolated lineage-specific neuroblasts for RNA sequencing.

125 lar and clonal data showing that all type II neuroblasts form in the embryo, produce INPs and express

126 er strains, we determined that DKK3 inhibits neuroblast formation by suppressing WNT signaling and Dk

127 ty in immature INPs suppresses supernumerary neuroblast formation in brat mutant brains.

128 r RTK-Ras signaling in the delamination of a neuroblast from an epithelial organ.

129 These droplets protect glia and also neuroblasts from peroxidation chain reactions that can d

130 re we show that the continuous supply of new neuroblasts from the subventricular zone is necessary fo

131 romoting Btd expression, thereby maintaining neuroblast functional heterogeneity.

132 Thus, Trx instructs a type II neuroblast functional identity by epigenetically promoti

133 Trx regulates a type II neuroblast functional identity in part by maintaining ch

134 type II neuroblasts gradually adopt a type I neuroblast functional identity, losing the competence to

135 ssary and sufficient for eliciting a type II neuroblast functional identity.

136 Most brain neuroblasts generate a series of ganglion mother cells (

137 e two neurons (type I lineage), but 16 brain neuroblasts generate a series of intermediate neural pro

138 In contrast, larval neuroblasts generate longer 50 division lineages, and c

139 and post-embryonic, in which the same set of neuroblasts give rise to the distinct larval and adult n

140 nt of the Drosophila central nervous system, neuroblasts go through two phases of neurogenesis separa

141 trx mutant type II neuroblasts gradually adopt a type I neuroblast function

142 blastoma tumor stroma is thought to suppress neuroblast growth via release of soluble differentiating

143 that substantial changes in the identity of neuroblasts have occurred during insect evolution.

144 Drosophila neural progenitors (neuroblasts) have been an excellent model for studying s

145 s critical for proper spindle positioning in neuroblasts, how Ana2 and LC8 interact is yet to be esta

146 l glia-like cells, intermediate progenitors, neuroblasts, immature neurons and neurons.

147 neurons (MNs) that are derived from a single neuroblast in Drosophila.

148 in ventriculomegaly with an increase of SVZ neuroblast in rostral migratory stream, whereas VEGF lig

149 lial-mesenchymal transition that mature into neuroblasts in a second proliferative zone.

150 ire of transcription factors expressed among neuroblasts in diverse patterns.

151 ilized zygotes in Caenorhabditis elegans and neuroblasts in Drosophila, and in the development of mam

152 from a limited number of progenitors, called neuroblasts in Drosophila.

153 Let-7 inhibition increases the proportion of neuroblasts in the cell cycle.

154 l death-levels and a decrease in SVZ-derived neuroblasts in the distal RMS, as compared to controls.

155 Neural stem cells or neuroblasts in the Drosophila melanogaster embryo delami

156 which innervate the inner ear, originate as neuroblasts in the floor of the otic vesicle and subsequ

157 to radial migration of postnatally generated neuroblasts in the olfactory bulb.

158 Spemann organizer, regulates delamination of neuroblasts in the otic vesicle.

159 s of Pbx1 expression in neuronally committed neuroblasts in the rostral migratory stream in a Pbx2 nu

160 n fails to form apical crescents in dividing neuroblasts in vivo, and the lack of Canoe phosphorylati

161 a glia-enriched conduit of forward-migrating neuroblasts in which chemorepulsive signals control the

162 tric division of a type II neural stem cell (neuroblast) in the Drosophila larval brain, the Brain tu

163 enitors that matured into neural stem cells (neuroblasts) in a second domain.

164 Ps), generated by type II neural stem cells (neuroblasts) in fly larval brains, provide an in vivo mo

165 ains the heterogeneity of neural stem cells (neuroblasts) in the developing Drosophila larval brain.

166 n Drosophila larval brain neural stem cells (neuroblasts) in which apoptosis is normally repressed.

167 ells in the medial OPC directly convert into neuroblasts, in an IPC subdomain they generate migratory

168 caused a near-absence of NEUROG1-expressing neuroblasts, increased cell death in the neurosensory ep

169 ivity also strongly suppresses supernumerary neuroblasts induced by overexpression of klu.

170 lear Prospero can drive proliferating larval neuroblasts into quiescence.

171 al drivers that are temporarily expressed in neuroblasts, into drivers expressed in all subsequent ne

172 discovered in Drosophila neural progenitors (neuroblasts) involve progenitor-intrinsic temporal trans

173 The other neuroblast is novel and appears to have arisen recently

174 neurons; the neuroepithelium that generates neuroblasts is also subdivided into six compartments by

175 sis and show how proliferation of individual neuroblasts is dictated by temporal and spatial cues.

176 transgenic mice, we find that the influx of neuroblasts is required for recovery of intrabulbar map

177 le neuroblastomas resemble mouse sympathetic neuroblasts lacking KIF1Bbeta independent of MYCN amplif

178 igate how hyperactivation of Notch in larval neuroblasts leads to tumours, we combined results from p

179 In neuroblasts, Lgl relocalizes to the cytoplasm at mitosis

180 for future comparative studies on individual neuroblast lineages in D. melanogaster and T. castaneum

181 ARCM labeling to identify all adult-specific neuroblast lineages in the late larval SEG and find a su

182 vidual cells from the developing otocyst and neuroblast lineages to assay 96 genes representing estab

183 SEG and find a surprisingly small number of neuroblast lineages, 13 paired and one unpaired.

184 ks that underlie the development of distinct neuroblast lineages, we marked and isolated lineage-spec

185 it results in the formation of novel ectopic neuroblast lineages.

186 izzy (fzy) gene that lead to premature brain neuroblast loss without perturbing cell proliferation in

187 Included were genes associated with the neuroblast maintenance and self-renewal programme that w

188 nscription factors that are likely to be pan-neuroblast, many transcription factors exist that are se

189 al stem cells (neuroblasts) to the published neuroblast map of the fruit fly Drosophila melanogaster.

190 The neuroblast map presented here can be used for future com

191 istochemistry to study the expression of the neuroblast marker doublecortin (DCX), and compared its e

192 ption factors, which have been implicated in neuroblast maturation.

193 f transcription factors present in different neuroblasts may govern the diverse lineage-specific neur

194 nges in the expression profile of individual neuroblasts might have contributed to the evolution of n

195 In the postnatal rodent brain, neuroblasts migrate long distances from the subependymal

196 at the S1P receptor 1 (S1P1) is expressed in neuroblasts migrating in the RMS.

197 oth pathways is required to ensure efficient neuroblast migration along the RMS.

198 and is best characterized for their roles in neuroblast migration during early embryogenesis.

199 stem cell niche organization and ultimately neuroblast migration in the anterior forebrain.SIGNIFICA

200 mily, as a molecule essential for tangential neuroblast migration in the postnatal mouse forebrain.

201 Neuroblast migration is a highly orchestrated process th

202 ial role for EphA4 in facilitating efficient neuroblast migration to the OB.

203 eration decrease, an increase in the eutopic neuroblast migration towards the olfactory bulb was obse

204 eam (RMS), yet are permissive to large-scale neuroblast migration.

205 ion occurs on demand and that its loss slows neuroblast migration.

206 stem characterized by interruption of normal neuroblasts migration between the 7(th) and 16(th) week

207 sms that govern the dynamic reshaping of the neuroblasts' morphology required for their migration alo

208 INP identity and enhances the supernumerary neuroblast mutant phenotype in brat mutant brains.

209 le exit of INPs in Drosophila larval type II neuroblast (NB) lineages.

210 In these regions, neuroblasts (NBs) divide asymmetrically to self-renew an

211 use quantitative live imaging of ingressing neuroblasts (NBs) in Drosophila melanogaster embryos to

212 During larval life most of the thoracic neuroblasts (NBs) in Drosophila undergo a second phase o

213 Here, we show that a subset of brain neuroblasts (NBs) in Drosophila utilize Phosphoinositide

214 Drosophila type II neuroblasts (NBs), like mammalian neural stem cells, dep

215 Drosophila neural stem cells, also known as neuroblasts (NBs), requires a 'decommissioning' phase th

216 uring asymmetric cell division of Drosophila neuroblasts (NBs).

217 erminates the self-renewal of larval type II neuroblasts (NBs, the Drosophila NSCs) and transforms ty

218 mmetrically dividing Drosophila melanogaster neuroblasts (NBs; neural stem cells).

219 In contrast, very little is known about neuroblasts, neural lineages, or any other aspect of the

220 nticle in the specification of an identified neuroblast (neuronal progenitor) lineage in the Drosophi

221 e II neuroblasts compared with non-selective neuroblasts, neurons and glia revealed a rich repertoire

222 oreover, we identified three thorax-specific neuroblasts not previously characterized and show that H

223 ctor Prospero is transiently detected in the neuroblast nucleus, followed by the establishment of a u

224 f PntP1 leads to both an increase in type II neuroblast number and the elimination of INPs.

225 Here, we identified the embryonic neuroblast origin of the adult neuronal lineages in the

226 By contrast, neuroblasts overexpressing the non-degradable form of ca

227 tically interact with erm to prevent type II neuroblast overgrowth.

228 rosophila cerebrum originates from about 100 neuroblasts per hemisphere, with each neuroblast produci

229 oxetine on proliferation of type II NSCs and neuroblast populations in the ventral hippocampus.

230 hin the ventral hippocampus, type II NSC and neuroblast populations specifically responded to fluoxet

231 Drosophila neuroblasts produce long, stereotyped lineages of neuron

232 Each neuroblast produces a specific neuronal lineage.

233 ut 100 neuroblasts per hemisphere, with each neuroblast producing a characteristic set of neurons.

234 rowth factor receptor activation to increase neuroblast production.

235 ts, into drivers expressed in all subsequent neuroblast progeny.

236 lt central complex, as do the larval type II neuroblast progeny?

237 characterize MYCN/ALK cooperation leading to neuroblast proliferation and survival that may represent

238 pports a function for SKP2 in the maintained neuroblast proliferation downstream of MYCN/ALK, which m

239 8A/B and Let-7 are essential for sympathetic neuroblast proliferation during normal development.

240 Therefore, Eyeless uncouples MB neuroblast proliferation from nutrient availability, all

241 xtrinsic factors control the reactivation of neuroblast proliferation in a fashion that has not yet b

242 In contrast, neuroblast proliferation is maintained when MYCN and ALK

243 ever, Lin28B overexpression neither sustains neuroblast proliferation nor affects let-7 expression.

244 ind that the glial cell niche also preserves neuroblast proliferation under conditions of hypoxia and

245 l function of MYCN and MYC in the control of neuroblast proliferation, as well as effects of overexpr

246 pregulation in a mouse model does not affect neuroblast proliferation, ganglion size, and Let-7 expre

247 e CDK inhibitor p27 for degradation, reduces neuroblast proliferation, implicating SKP2 in the mainta

248 g neurogenesis and is important for in vitro neuroblast proliferation.

249 functions for endogenous Lin28 and Let-7 in neuroblast proliferation.

250 n had a similar effect, leading to decreased neuroblast proliferation.

251 ing: nutritional cues regulate the timing of neuroblast proliferation/quiescence and a steroid hormon

252 w level nuclear Prospero precedes entry into neuroblast quiescence even when the timing of quiescence

253 Yet the origin of type II neuroblasts remains mysterious: do they form in the embr

254 ssion of the Ecdysone receptor in mid-larval neuroblasts, rendering them competent to respond to the

255 Ps (imINPs), whereas the increase in type II neuroblasts results from the dedifferentiation of imINPs

256 rough changes in gene expression in a single neuroblast reveals a surprising capacity for novel circu

257 ttenuated competence to respond to all known neuroblast self-renewal factors in INPs.

258 la embryonic development, neural stem cells (neuroblasts) sequentially express transcription factors

259 These cues enforce strict neuroblast spatial boundaries within the dense astroglia

260 in tumor model using brat-RNAi driven by the neuroblast-specific promoter inscuteable Suppressing Bra

261 ian T cell differentiation in the thymus and neuroblast specification in Drosophila are both regulate

262 ogical and molecular analyses pinpointed the neuroblast stage as the main developmental window when t

263 ed in the cleavage furrow of the Q.a and Q.p neuroblasts, suggesting that TOE-2 might position the cl

264 but inhibition later significantly increases neuroblast survival.

265 increased proliferation but does not sustain neuroblast survival.

266 l axes generate this neuronal diversity: all neuroblasts switch fates over time to produce different

267 extrinsic pathways that regulate Drosophila neuroblast temporal patterning: nutritional cues regulat

268 ther pediatric cancers, does not evolve from neuroblasts that continue to divide and involves Let-7-i

269 Drosophila central neurons arise from neuroblasts that generate neurons in a pair-wise fashion

270 One area where neuroblasts that give rise to adult-born neurons are gen

271 Interestingly, neuroblasts that maintain initial Imp/Syp levels can sti

272 amplifying cells (TACs), which give rise to neuroblasts that migrate to the olfactory bulb.

273 the ventricular-subventricular zone generate neuroblasts that migrate via the rostral migratory strea

274 was a significant reduction in the number of neuroblasts that reached the OB and integrated into the

275 c stem cell niche generates highly migratory neuroblasts that transit the anterior forebrain along a

276 In almost all neuroblasts the relative positions in the ventral hemi-n

277 are conserved; however, in over half of the neuroblasts the time of formation as well as the gene ex

278 In Drosophila neuroblasts, the Inscuteable/Baz/Par-6/aPKC complex recr

279 Unlike TFs expressed in mitotically active neuroblasts, these TFs do not regulate each other's expr

280 within the pathway and efficient transit of neuroblasts through the anterior forebrain to the olfact

281 he survival and migration of newly generated neuroblasts through the RMS to the olfactory bulb.

282 We labeled particular neuroblasts throughout neurogenesis by activating a cond

283 Here, we use chick sympathetic neuroblasts to examine the normal function of MYCN and M

284 reate coarse temporal windows within type II neuroblasts to pattern INPs, which subsequently undergo

285 and expression profile of neural stem cells (neuroblasts) to the published neuroblast map of the frui

286 n immature INPs by repressing genes encoding neuroblast transcriptional activators.

287 poral fating mechanisms, we profiled type II neuroblasts' transcriptome across time.

288 ular transition is known: Chinmo/Imp/Lin-28+ neuroblasts transition to Syncrip+ neuroblasts.

289 tiates T cell leukemia as well as Drosophila neuroblast tumors.

290 ther, the results suggest that Notch induces neuroblast tumours by directly promoting the expression

291 We show that retinal neuroblasts undergo fast oscillations and that myosin co

292 malian neural stem cells, Drosophila type II neuroblasts utilize INPs to produce neurons and glia.

293 hat Nogo-A-Delta20 promotes the migration of neuroblasts via HSPGs but not S1PR2.

294 the OB; however, upon arrival to the OB, the neuroblasts were distributed aberrantly within the radia

295 The targeted neuroblasts were efficiently recovered using a custom-bu

296 t migration of both early-born and late-born neuroblasts, which could be linked to reduced reelin sig

297 ifically affects the asymmetrically dividing neuroblasts, which display supernumerary centrosomes and

298 However, a small subset, the mushroom body neuroblasts, which generate neurons important for memory

299 lows long-term proliferation and survival of neuroblasts with differentiated characteristics.

300 Ablating neuroblasts with hydroxyurea (HU) prior to onset of larv