ライフサイエンスコーパス: daughter cell

1 one set of sister chromatids to each nascent daughter cell.

2 self-renewed stem cell and a differentiating daughter cell.

3 ell size, yielding a smaller differentiating daughter cell.

4 ing SPEECHLESS for degradation in the larger daughter cell.

5 nes are enriched towards the differentiating daughter cell.

6 leading to their inheritance by the germline daughter cell.

7 elf-renewing stem cell and a differentiating daughter cell.

8 g to the retention of seam cell fate in both daughter cells.

9 tin at the intercellular bridges between GSC-daughter cells.

10 mulation and asymmetric partitioning between daughter cells.

11 viral genomes to hitchhike or piggyback into daughter cells.

12 enome and divide the duplicated DNA into two daughter cells.

13 ependent segregation of mitochondria between daughter cells.

14 e elongation and position chromosomes within daughter cells.

15 gate the origin of replication region to new daughter cells.

16 aughter cells but is repressed in hypodermal daughter cells.

17 process of equal chromosome segregation into daughter cells.

18 hfully passed on through many generations of daughter cells.

19 actile ring drives the separation of the two daughter cells.

20 s, localize to puncta and associate with the daughter cells.

21 ce that contributes to PM ingression between daughter cells.

22 ced state in the mother cell is inherited in daughter cells.

23 ion that remodels the parental cell into two daughter cells.

24 rpC redistributes to the growing edge of the daughter cells.

25 osin contractile ring that separates the two daughter cells.

26 y regulated partitioning of chromosomes into daughter cells.

27 torial furrowing and separation into the two daughter cells.

28 consequently, abnormal bud-site selection in daughter cells.

29 ng increasing mRNA synthesis rate in smaller daughter cells.

30 a severe decline of replicative life span of daughter cells.

31 es of gametes, zygotes, and apical and basal daughter cells.

32 eposition of a new cell wall between the two daughter cells.

33 lusively determines cell-cycle commitment in daughter cells.

34 nd equally segregate its genome into two new daughter cells.

35 cular vascular plexus, and then divided into daughter cells.

36 of cytoplasmic connections between dividing daughter cells.

37 aused premature formation of deposits in the daughter cells.

38 nd results in the physical separation of two daughter cells.

39 on have significant effects on the resulting daughter cells.

40 eostasis, and chromosome distribution within daughter cells.

41 ntrols septal PG synthesis and separation of daughter cells.

42 ayer of separating membranes between the two daughter cells.

43 triggers petite formation preferentially in daughter cells.

44 division and appropriate differentiation of daughter cells.

45 o create the new cell poles of the separated daughter cells.

46 an internal cue for establishing PCP in new daughter cells.

47 oviding a simple way to ensure equally sized daughter cells.

48 their chromosomes and partition them to two daughter cells.

49 ired for their proper segregation to the two daughter cells.

50 l repartition of chromosomes between the two daughter cells.

51 inant control mechanism for S phase entry of daughter cells.

52 e products of which proceeded to form viable daughter cells.

53 DSB at ori5, preventing mtDNA segregation to daughter cells.

54 arate replicated chromosomes accurately into daughter cells.

55 for asymmetric division and rejuvenation of daughter cells.

56 induced cyclin D1 (CCND1) mRNA to newly born daughter cells.

57 ation is passed on to the next generation of daughter cells.

58 n asymmetric cell division yielding distinct daughter cells.

59 ures accurate segregation of chromatids into daughter cells.

60 cate sufficient raw material to generate two daughter cells.

61 hromosome dimers during their segregation to daughter cells.

62 e equal division of genetic material between daughter cells.

63 of events by which a cell gives rise to two daughter cells.

64 and lowered SPCH abundance in one of the two daughter cells.

65 slation, and facilitate the transport to the daughter cells.

66 o physically cleave the mother cell into two daughter cells.

67 r the final abscission and separation of the daughter cells.

68 sentangling and delivery of DNA molecules to daughter cells.

69 dramatic shape change as it divides into two daughter cells.

70 ned to mitosis, it resulted in aneuploidy in daughter cells.

71 ides the chromosomes between the two nascent daughter cells.

72 catalyzes membrane cleavage to create equal daughter cells.

73 ucleus formation and increased aneuploidy in daughter cells.

74 nt must also be properly distributed between daughter cells.

75 how BASL differentially functions in the two daughter cells.

76 per separation of the cell contents into two daughter cells.

77 dividing cell wall to separate newly formed daughter cells.

78 r the generation of two viable and identical daughter cells.

79 he cell cycle is crucial to generate healthy daughter cells.

80 pherally at the apical surface of one of the daughter cells.

81 re and faithfully segregate chromosomes into daughter cells.

82 is leading to the physical separation of the daughter cells.

83 to ensure the correct separation of the two daughter cells.

84 of sister chromatids to each of the nascent daughter cells.

85 tosis, and cell division, producing up to 16 daughter cells.

86 s manner, LytN facilitates the separation of daughter cells.

87 d the accurate segregation of chromosomes to daughter cells.

88 te and eventually pinch off to form separate daughter cells.

89 arental chromosomes into a single nucleus in daughter cells.

90 rrow ingression and led to frequent lysis of daughter cells.

91 ansient protein structure connecting the two daughter cells.

92 mmetry and differential cell fate of the two daughter cells.

93 some unlinking and faithful segregation into daughter cells.

94 r released or rapidly degraded by one of the daughter cells.

95 differentiated, effector-molecule-expressing daughter cells.

96 ought to be formed de novo in the developing daughter cells.

97 itioning of cellular components into the two daughter cells.

98 ithful segregation of the genome between two daughter cells.

99 sis, with GSCs failing to abscise from their daughter cells.

100 chromosome distribution into the two forming daughter cells.

101 and accurate segregation of chromosomes into daughter cells.

102 ansmission of altered genetic information to daughter cells.

103 Geminin family members modulate the fate of daughter cells.

104 cess, producing two morphologically distinct daughter cells.

105 tep of mitosis that physically separates two daughter cells [1, 2].

106 site where they build the partition between daughter cells(2-4).

107 h of the septum to form the new poles of the daughter cells(4).

108 cause BASL polarity is only exhibited by one daughter cell after an asymmetric cell division, we stud

109 herichia coli, FtsEX is required to separate daughter cells after cell division and for viability in

110 n in rDNA is highly correlated in mother and daughter cells after cell division, indicating that the

111 ants are observed at the apical membranes of daughter cells and are much more abundant in early-stage

112 replicated chromosomes are partitioned into daughter cells and can serve as a platform for the re-es

113 ssion, the process that physically separates daughter cells and completes cell division.

114 egregation, triggering DNA damage in diploid daughter cells and elevated ploidy.

115 It controls the final separation of the daughter cells and has been involved in cell fate, polar

116 accurate partition of the cytoplasm between daughter cells and the correct localization of the daugh

117 ols the proliferation-quiescence decision in daughter cells and thereby couples protein production wi

118 thousands of individual pairs of mother and daughter cells and track their fates.

119 iminate transmission of mRNAs from mother to daughter cells, and favors the response capacity of the

120 of the mother cell are partitioned into the daughter cells, and how the daughters are positioned wit

121 ve to errors in partitioning of volume among daughter cells, and not surprisingly, this process is we

122 faithful distribution of chromosomes between daughter cells, and spindle orientation is a major deter

123 Importantly, NPC-derived daughter cells appeared to be latently infected with HIV

124 Therefore, two daughter cells are differentiated by BASL polarity-media

125 In particular, budding yeast daughter cells are more vulnerable to stresses than the

126 ony-a process wherein components for several daughter cells are produced within a common cytoplasm an

127 e final stage of cell division where the two daughter cells are separated, is mediated by the endosom

128 red in partitioning of molecules between two daughter cells are significant.

129 elf-renew, clonally yielding a TCF1-silenced daughter cell as well as a sibling cell maintaining TCF1

130 esis, the midbody is inherited by one of the daughter cells as a remnant that initially locates perip

131 region compromised segregation of TR DNA to daughter cells, as assessed by retention of green fluore

132 Paired daughter cell assays demonstrate that Asxl2 loss enhance

133 ation being synchronous and coordinated with daughter cell assembly(2,3).

134 Our data reinforce the importance of daughter-cell-associated factors and centrosome-based re

135 and, surprisingly, loss of viability of one daughter cell at division, suggesting specific impairmen

136 ts, which can segregate cleanly to different daughter cells at anaphase.

137 n, culminating in the physical separation of daughter cells at the end of mitosis.

138 at the intercellular bridge between the two daughter cells at the end of mitosis.

139 of amoebas, fungi, and animal cells into two daughter cells at the end of the cell cycle depends on a

140 other cell produces only a limited number of daughter cells before it slows division and dies.

141 n, acting as a contractile ring to establish daughter cell boundaries.

142 4), is selectively induced in alae-secreting daughter cells but is repressed in hypodermal daughter c

143 pigenetic information is transmitted only to daughter cells, but evidence is emerging, in both verteb

144 the region reduced segregation of TR DNA to daughter cells, but not episome maintenance.

145 heir accurate segregation and propagation to daughter cells, but the mechanisms ensuring coordination

146 centrosome loss prevent the growth of unfit daughter cells by activating a pathway involving 53BP1,

147 tric and asymmetric cell divisions producing daughter cells capable of self-renewal.

148 n the differences in c-Myc expression in one daughter cell compared to the other.

149 Thus, daughter cells control the proliferation-quiescence deci

150 flows from the ring and enriches the nascent daughter cell cortices.

151 that all intestinal regeneration arises from daughter cell dedifferentiation, marking the coming-of-a

152 After mitosis, fate-committed daughter cells delaminate from this germinative zone.

153 Daughter cells derived from PGCCs showed attenuated capa

154 The developmental asymmetry of fission yeast daughter cells derives from inheriting 'older Watson' ve

155 l indeed biases stochastic fate decisions of daughter cells despite mitotic rounding.

156 ling from the SPB that is delivered into the daughter cell (dSPB) during anaphase and the SPB that re

157 and divide in order to be inherited by each daughter cell during mitosis.

158 he genome has partitioned between mother and daughter cells during anaphase.

159 chinery for the transmission of propagons to daughter cells during cell division and cytoplasmic tran

160 the duplicated cellular organelles into two daughter cells during cell division, a process known as

161 ins become asymmetrically inherited by outer daughter cells during cell division, where they stabiliz

162 to gene expression that can be passed on to daughter cells during cell division, whereas RNAi does n

163 idases that participate in the separation of daughter cells during cell division.

164 MiQ aggregate deposit was not transferred to daughter cells during cell division.

165 Force plays a central role in separating daughter cells during cytokinesis, the last stage of cel

166 ferentiation and the relative positioning of daughter cells during development.

167 ursors and prevents them from spreading into daughter cells during division by subjecting them to the

168 or disassembly, and their partitioning among daughter cells during division.

169 n of the chromosomal content between the two daughter cells during division.

170 roper segregation of the genetic material to daughter cells during mitosis and meiosis.

171 faithful distribution of chromosomes between daughter cells during mitosis as well as for other cellu

172 accurate segregation of genetic material to daughter cells during mitosis depends on the precise coo

173 To segregate the episomes into daughter cells during mitosis, they are tethered to cell

174 equal segregation of duplicated DNA into two daughter cells during mitosis.

175 stack is duplicated and partitioned into two daughter cells during the cell cycle of the protozoan pa

176 omolecules (such as RNAs and proteins) among daughter cells during the division of a cancer cell.

177 ount for the cell shape and demonstrate that daughter cells emerging from wave-mediated cytofission e

178 After mitosis, the majority of daughter cells extend a long, basally oriented filopodia

179 ar diversity and defects can lead to altered daughter cell fates and numbers.

180 d to chemotherapy-induced damage by altering daughter cell fates.

181 stomatal lineage but is inherited equally by daughter cells following an asymmetric cell division.

182 cient segregation of the viral genome to the daughter cells following cell division.

183 ead, DNA lesions segregate, unrepaired, into daughter cells for multiple cell generations, resulting

184 gets mRNAs acquired in the nucleus either to daughter cells for translation or to stress granules (SG

185 f dividing Chlamydia trachomatis cells where daughter cell formation occurs, and peptidoglycan regula

186 tric cell division to ensure the fidelity of daughter cell formation.

187 ing cell division is critical for preventing daughter cells from inheriting an abnormal number of chr

188 nvironment contains sufficient resources for daughter cell generation.

189 at facilitate polarized vesicle delivery and daughter cell growth.

190 but the process arrests at an early stage of daughter cell growth.

191 n of CDK1-driven mitotic translation reduces daughter cell growth.

192 DNA asymmetrically, preferentially into the daughter cell harboring the young centrosome.

193 active transcriptional states from mother to daughter cells has the potential to foster precision in

194 terphase expression pattern is transduced to daughter cells have been unclear.

195 and, upon partitioning, reassembles in each daughter cell; however, it is not clear whether the disa

196 Successful separation of two daughter cells (i.e., cytokinesis) is essential for life

197 s complete mitosis, a fraction of newly born daughter cells immediately enter the next cell cycle, wh

198 ith symmetrical distribution of viral DNA to daughter cells.IMPORTANCE A mechanistic understanding of

199 ir integrity and are inherited by developing daughter cells in a She2p/She3p-dependent manner.

200 on of [PSI(+) ] propagons between mother and daughter cells in a sub-population of cells during cell

201 i of cells; partitioning the viral genome to daughter cells in dividing cells; avoiding recognition b

202 -lived growth differences between mother and daughter cells in the presence of subinhibitory drug con

203 f cell division that defines the position of daughter cells in the tissue.

204 number plasmids, diffusion ensures that both daughter cells inherit plasmids after cell division.

205 assembly checkpoint (SAC) ensures that each daughter cell inherits an identical set of chromosomes.

206 divisions, which are highly asymmetric: one daughter cell inherits the vacuole, the other the growin

207 Every daughter cell inherits two things from its mother: genet

208 ance proliferation with the incorporation of daughter cells into organ primordia.

209 cell in two identical halves can be used in daughter cells, irrespective of its orientation in relat

210 oning duplicated chromosomes equally between daughter cells is a microtubule-mediated process essenti

211 ell lineages, the precise differentiation of daughter cells is critical to maintain tissue homeostasi

212 HO expression in daughter cells is inhibited by high concentration of Ash

213 Faithful segregation of chromosomes to two daughter cells is regulated by the formation of a bipola

214 Cytokinesis-the division of a cell into two daughter cells-is a key step in cell growth and prolifer

215 he cell cycle before symmetric division into daughter cells, leading to polyploidy and multinucleatio

216 tioning of the replicated chromosomes to the daughter cells (M phase) during eukaryotic cell division

217 ng the cleavage plane are pulled between the daughter cells, making a new interface between neighbors

218 Because of this movement, daughter cells may be born displaced from the tissue lay

219 n clearance, and the physical sealing of the daughter cell membranes.

220 sma membrane in the furrow, and separate the daughter cell membranes.

221 ial amino acids to generate large numbers of daughter cells necessary for effective immunity to patho

222 mitotic chromosomes to segregate genomes to daughter cell nuclei.

223 mes and TR DNA to segregate virus genomes to daughter cell nuclei.

224 Here, we show that most growth of a new daughter cell occurs in mitosis.

225 echanism, the asymmetric distribution to the daughter cell of the mRNA for a specific glucose transpo

226 To examine in detail differences between the daughter cells of a proliferative division of procyclic

227 erminants, ensuring asymmetric division into daughter cells of different fates.

228 of cells that divide asymmetrically to give daughter cells of different size and fate.

229 body remnants are more often retained on the daughter cells of early proliferative divisions.

230 of adult cells and demonstrate that the two daughter cells of many early embryonic cell-doubling eve

231 During brain development, the daughter cells of neural stem cells have to make a choic

232 romatin-bridge formation, and micronuclei in daughter cells of proband skin fibroblasts.

233 tudies indicate that replicative lifespan in daughter cells of Sacchraromyces cerevisiae depends on t

234 is, which enables the physical separation of daughter cells once mitosis has been completed, is execu

235 observe defects in cell-cell communication, daughter cell orientation and the juxtanuclear accumulat

236 Spindles polarized, pairs of daughter cells oriented between the DTC and Sh1, and Sh1

237 ne, NR4A3 that was downregulated in MKN28 GC daughter cells overexpressing a constitutively activated

238 Erythroid progenitor daughter cell pairs have similar transcriptomes with or

239 Daughter cell positions can be specified via orienting t

240 selectively required for the maintenance of daughter cells produced by castration-resistant Nkx3.1-e

241 o important for subsequent progenitor and/or daughter cell proliferation in the brain.

242 l as 'hyper-proliferation' of progenitor and daughter cells, promoted by PRC2-mediated repression of

243 ndergo asymmetric cell division, wherein the daughter cell proximal to the APC is more likely to diff

244 nes involved in the growth and rebuilding of daughter cells, rather than cell type-specific functions

245 How do daughter cells re-establish the original transcription p

246 ransmitted through cell division such that a daughter cell recapitulates the spatial genome organizat

247 Daughter cells received equal shares of preinitiation fa

248 ions retract their basal processes, and both daughter cells regrow a new process following cytokinesi

249 anscriptional memory and reactivation in the daughter cells remain unclear.

250 regation of protein aggregates by mother and daughter cells remains controversial, in part because of

251 that the OPC-enriched gene, PCDH15, mediates daughter cell repulsion and facilitates proliferation.

252 dicated that flagella-based forces initiated daughter cell separation and provided a source for membr

253 t amidase activity alone is insufficient for daughter cell separation and that lytic transglycosylase

254 1 in regulating neural progenitor cell (NPC) daughter cell separation.

255 lity is tightly controlled to execute proper daughter cell separation.

256 ds of division are dynamically determined by daughter cell shape.

257 es phenotypic differences between mother and daughter cells similar to other pathogenic yeasts.

258 hydrolyse crosslinked peptidoglycan between daughter cells so that they can separate(7).

259 sembly of a contractile ring, which promotes daughter cell splitting.

260 boost of egl-1 that occurs specifically in a daughter cell that is programmed to die.

261 threshold necessary to trigger death only in daughter cells that are programmed to die.

262 ing that there may be glycan bridges between daughter cells that cannot be resolved by amidases.

263 s in a short pulse of ERK inactivity in both daughter cells that correlates with elevated endpoint NA

264 al features: unequal cell division producing daughter cells that elongate with different velocities,

265 ate within a parasitophorous vacuole to form daughter cells that eventually exit (egress) by sequenti

266 undergo asymmetric division, giving rise to daughter cells that exhibit distinct tendencies to adopt

267 After stem cell division, daughter cells that exit the stem cell domain acquire tr

268 nequally distributing factors to the nascent daughter cells that influence their eventual fate toward

269 tric divisions, increasing the proportion of daughter cells that inherit high amounts of effector fat

270 ments divide asymmetrically, producing short daughter cells that tend to be devoid of damage and have

271 ofound loss of division symmetry, generating daughter cells that vary widely in size and eventually g

272 to the production of properly sized, viable daughter cells, the mechanisms underlying division site

273 nformation is segregated reliably to the two daughter cells through cell division.

274 ic information is transmitted from mother to daughter cells through mitosis.

275 re required for faithful transmission to the daughter cell to accurately maintain cell identity durin

276 ll division while simultaneously programming daughter cells to adopt diverging fates in a spatially s

277 This additionally allows the daughter cells to be born damage free.

278 lly duplicated and accurately transmitted to daughter cells to preserve cell identity during the cell

279 alignment of the mitotic spindle allows the daughter cells to stay within the epithelium.

280 Feedback signals from daughter cells to stem cells are well studied and known

281 y, the PPARgamma-homologue Eip75B drives ISC daughter cells towards absorptive enterocyte lineage ens

282 ral and spatial control to produce different daughter cell types in proper numbers and sequence.

283 All daughter cell types of engineered NSCs (neurons, astrocy

284 se, when sister chromatids must transit into daughter cells uninterrupted.

285 ytoplasmic components determines the fate of daughter cells upon asymmetric division.

286 d to ensure equal chromosome distribution in daughter cells upon mitosis.

287 complete separation and isolation of the two daughter cells via abscission.

288 h activation of senescence, while budding of daughter cells was associated with senescence escape.

289 d frequency at which circles redistribute to daughter cells was not due to changes of anaphase durati

290 n factories toward the tip of the developing daughter cell, where protein synthesis is most heavily r

291 basement membrane is lost in differentiating daughter cells, where YAP and TAZ become mostly cytoplas

292 remodeling, especially during separation of daughter cells, which depends heavily upon the activity

293 cell divisions and generate a core of small daughter cells, which is a prerequisite for lateral root

294 ly, proliferative cell divisions produce two daughter cells, which look similar but are not identical

295 , repair them, or avoid their propagation to daughter cells, which would be particularly detrimental

296 compact, as required for clean separation to daughter cells, while maintaining close parallel alignme

297 Stem cells produced daughter cells with an extraordinarily high rate of turn

298 on generates cellular diversity by producing daughter cells with different fates.

299 iability each time a cell divides, producing daughter cells with different sizes and growth rates.

300 e replicated copies of their genome to their daughter cells with extremely high fidelity.

301 a stable cytoplasmic bridge between the two daughter cells, Z2 and Z3 Depletion of several regulator