ライフサイエンスコーパス: daughter cell

1 ing SPEECHLESS for degradation in the larger daughter cell.

2 he maternal or paternal chromosomes, in each daughter cell.

3 ritance, ER protein aggregates can enter the daughter cell.

4 symmetric between ISC and its differentiated daughter cell.

5 restrict ERK1/2 activation to the posterior daughter cell.

6 ell size, yielding a smaller differentiating daughter cell.

7 y regulated partitioning of chromosomes into daughter cells.

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

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

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

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

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

13 sentangling and delivery of DNA molecules to daughter cells.

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

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

16 ides the chromosomes between the two nascent daughter cells.

17 catalyzes membrane cleavage to create equal daughter cells.

18 ucleus formation and increased aneuploidy in daughter cells.

19 how BASL differentially functions in the two daughter cells.

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

21 dividing cell wall to separate newly formed daughter cells.

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

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

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

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

26 d defects in the generation of unequal-sized daughter cells.

27 olase responsible for physical separation of daughter cells.

28 SCs), as mutations are readily propagated to daughter cells.

29 ion aged mitochondria asymmetrically between daughter cells.

30 ss leading to the physical separation of two daughter cells.

31 chromosomes must be precisely partitioned to daughter cells.

32 omponents that confer distinct cell fates to daughter cells.

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

34 s determined as the mother cell divides into daughter cells.

35 per segregation of the broken fragments into daughter cells.

36 tal for faithful chromosome segregation into daughter cells.

37 lusively determines cell-cycle commitment in daughter cells.

38 sting walls and divides the cytoplasm of the daughter cells.

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

40 enables the segregation of replicated DNA to daughter cells.

41 50-200 mum chromatin bridges connecting the daughter cells.

42 e segregation and inflicts DNA damage on the daughter cells.

43 ls in quadrants, generating asymmetry in the daughter cells.

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

45 ore division, after which it splits into two daughter cells.

46 s to reduce transmission of DNA damage to G1 daughter cells.

47 sis when a mother cell is separated into two daughter cells.

48 of cytoplasmic connections between dividing daughter cells.

49 s of mitosis and how cells divide to produce daughter cells.

50 enhancing cooperation than division into two daughter cells.

51 aused premature formation of deposits in the daughter cells.

52 sulting in efficient random partition to the daughter cells.

53 er cells, but is largely absent from nascent daughter cells.

54 at segregates the duplicated genome into two daughter cells.

55 t are faithfully and robustly regenerated in daughter cells.

56 l segregation of duplicated chromosomes into daughter cells.

57 me substrates is differentially regulated in daughter cells.

58 be faithfully replicated and transmitted to daughter cells.

59 equal centrosome/centriole segregation into daughter cells.

60 and to prevent segregation of plasmid DNA to daughter cells.

61 the transmission of extensive DNA damage to daughter cells.

62 in aging mother cells, but is more acidic in daughter cells.

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

64 1 mutant, Ace2 is present in both mother and daughter cells.

65 somes before their ultimate segregation into daughter cells.

66 stribution of the duplicated genome into two daughter cells.

67 on have significant effects on the resulting daughter cells.

68 eostasis, and chromosome distribution within daughter cells.

69 ntrols septal PG synthesis and separation of daughter cells.

70 ayer of separating membranes between the two daughter cells.

71 triggers petite formation preferentially in daughter cells.

72 division and appropriate differentiation of daughter cells.

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

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

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

76 their chromosomes and partition them to two daughter cells.

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

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

79 l repartition of chromosomes between the two daughter cells.

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

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

82 ng increasing mRNA synthesis rate in smaller daughter cells.

83 arate replicated chromosomes accurately into daughter cells.

84 for asymmetric division and rejuvenation of daughter cells.

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

86 n asymmetric cell division yielding distinct daughter cells.

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

88 ures accurate segregation of chromatids into daughter cells.

89 cate sufficient raw material to generate two daughter cells.

90 hromosome dimers during their segregation to daughter cells.

91 e equal division of genetic material between daughter cells.

92 ell phenotype) and inefficient separation of daughter cells (a chaining phenotype).

93 m generates less than one hemisphere of each daughter cell, a trait we show is common to other cocci.

94 After asymmetric division, the ee daughter cell acts as a source of Dl that induces low No

95 and one does not-or symmetric, in which both daughter cells adopt the same fate, either stem or non-s

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

97 t associates with septin rings on mother and daughter cells after cell separation.

98 to be incorporated into a single nucleus in daughter cells after mitosis.

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

100 centrosomes influences SYS-1 inheritance in daughter cells and cell-fate outcomes after ACD.

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

102 1 increases cytosolic proton availability in daughter cells and facilitates vacuole re-acidification

103 rmines the relative size and position of the daughter cells and influences the asymmetric inheritance

104 ions the cytoplasm of a parent cell into two daughter cells and is essential for the completion of ce

105 rect segregation of genetic information into daughter cells and maintain genome integrity.

106 e RlpA is needed for efficient separation of daughter cells and maintenance of rod shape.

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

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

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

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

111 Ace2 normally accumulates only in daughter cells, and only activates transcription in daug

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

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

114 otic cell cycle is cytokinesis, when two new daughter cells are born.

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

116 stem cell maintenance, while differentiated daughter cells are known to provide feedback signals to

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

118 ast is asymmetric-mother cells age but their daughter cells are rejuvenated.

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

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

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

122 s overlap, and its nucleoid is segregated to daughter cells as a forked DNA circle with replication o

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

124 protein that normally accumulates mostly in daughter cells; Ash1 is a transcriptional repressor, and

125 Paired daughter cell assays demonstrate that Asxl2 loss enhance

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

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

128 omous replication and efficient partition to daughter cells at cell division.

129 ilitates analysis of protein partitioning to daughter cells at division, revealing a broad and robust

130 E. coli usually proceeds symmetrically, with daughter cells at roughly 180 degrees to each other.

131 the intercellular membrane bridge connecting daughter cells at the end of cytokinesis.

132 mbrane to promote the physical separation of daughter cells at the end of mitosis, is sequestered in

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

134 icated chromosomes are evenly distributed to daughter cells at the metaphase-anaphase transition.

135 16-cell stage embryo determines the fate of daughter cells, based on how asymmetrically distributed

136 divisions by analysing only the mean size of daughter cells, because their means can be the same.

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

138 This results in smaller daughter cells being born with higher Whi5 concentration

139 tosis is required for their segregation into daughter cells but must be reversed to allow for postmit

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

141 Cytokinesis generally produces two separate daughter cells, but in some tissues daughter nuclei rema

142 n bacteria, some plasmids are partitioned to daughter cells by assembly of actin-like proteins (ALPs)

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

144 investigated real-time actin assembly during daughter cell-cell adhesion formation in human breast ep

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

146 ect of cell division as it ensures that each daughter cell contains a single nucleus.

147 Thus, daughter cells control the proliferation-quiescence deci

148 ivide symmetrically and that both mother and daughter cells convert into reactive astrocytes.

149 roles in equal segregation of DNA content to daughter cells, coordination of growth and differentiati

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

151 wo dozen distinct mRNAs from yeast mother to daughter cell cytoplasm is a classical paradigm for euka

152 Daughter cells derived from PGCCs showed attenuated capa

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

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

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

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

157 ery mediates the physical separation between daughter cells during cytokinetic abscission.

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

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

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

161 are essential and must be transmitted to the daughter cells during division.

162 inheritance of the Golgi apparatus into the daughter cells during each cycle of cell division is med

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

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

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

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

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

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

169 viors, including proliferative potential and daughter cell fates, may contribute to variations in cor

170 Splitting of the cell into two daughter cells followed a local softening of the cell wa

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

172 es and continuously generate differentiating daughter cells for production of spermatozoa.

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

174 en shown to play a role in asexual T. gondii daughter cell formation, yet the mechanism is unknown.

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

176 to the IMC to ensure correct progression of daughter cell formation.

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

178 nvironment contains sufficient resources for daughter cell generation.

179 at facilitate polarized vesicle delivery and daughter cell growth.

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

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

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

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

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

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

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

187 t airway basal stem cells maintain secretory daughter cells in airway epithelia through forward regul

188 hat AmiA from Chlamydia pneumoniae separates daughter cells in an Escherichia coli amidase mutant.

189 ture that segregates chromosomes to generate daughter cells in mitosis or haploid gametes in meiosis.

190 known to form a boundary between mother and daughter cells in mitosis, but their role in other morph

191 dynamic landscape to promote organization of daughter cells in the context of the three-dimensional g

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

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

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

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

196 inesis is often asymmetric, in that only one daughter cell inherits the midbody ring (MR) upon comple

197 Vertical daughter cells initiated an unpolarized cell population

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

199 Size of daughter cells is a key factor to regulate cell division

200 regation of duplicated genetic material into daughter cells is critical to all organisms.

201 ate their inheritance during partitioning to daughter cells is less well understood.

202 example, division of a proto-cell into many daughter cells is more powerful in enhancing cooperation

203 distribution of the ribosomes among the new daughter cells is often unequal.

204 he MinP protein in pXO1 distribution between daughter cells is proposed.

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

206 pies of its chromosome for partitioning into daughter cells is unknown, partly due to the difficulty

207 ble cell lines, CRISPR/Cas9 enhancer-deleted daughter cell lines, transient transfection/mutagenesis

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

209 NA is replicated (S) and partitioned between daughter cells (M).

210 forward signal is shown to be necessary for daughter cell maintenance.

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

212 gs, IPF mesenchymal progenitor cells produce daughter cells manifesting the full spectrum of IPF hall

213 For example, following cell division the two daughter cells may not fully separate but stay attached

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

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

216 omes in anaphase and their delivery into the daughter cells needs to be accurately executed to mainta

217 em/progenitor cell can serve as a functional daughter cell niche.

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

219 the final step in the physical separation of daughter cells occurs.

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

221 e cleavage furrow asymmetrically to generate daughter cells of different sizes.

222 orms lingual epithelial cell fate, such that daughter cells of lingual epithelial progenitors form ce

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

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

225 ering leads to asymmetric cell divisions and daughter cells of unequal size; in contrast, if the chec

226 o the need for segregation of arrays between daughter cells on division, ensuring the production of c

227 ls divide asymmetrically, giving rise to two daughter cells, one of which retains the parent cell sel

228 eroplasmy is stably maintained in individual daughter cells over multiple cell divisions.

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

230 Finally, analysis of daughter-cell pairs and isogenic populations indicates t

231 ly during cytokinesis and abscission, when 2 daughter cells partition through coordinated actomyosin

232 However inhibition of COX-2 in daughter cells prevented sphere formation, indicating a

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

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

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

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

237 ergent-extension, mitotic cell division, and daughter cell rearrangement do not contribute significan

238 must be faithfully segregated to ensure that daughter cells receive one copy of each chromosome.

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

240 divisions are either asymmetric-in which one daughter cell remains a stem cell and one does not-or sy

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

242 ue of human Angiopoietin, in differentiating daughter cells renders germline stem cells sensitive to

243 or the transmission of shape from parent to daughter cells requires existing wall material as a temp

244 the distribution of the chromosomes into the daughter cells requires the degradation of cyclin B.

245 After cytokinesis, the daughter cells respread into matrix voids and invaded th

246 cting mitosis in an unperturbed manner, both daughter cells return to the confinement of the pillars.

247 non-essential, this activity is critical for daughter cell separation and outer membrane invagination

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

249 Thus, the ultrafast daughter cell separation in S. aureus appears to be driv

250 in Saccharomyces cerevisiae prevents mother-daughter cell separation, generating multicellular 'snow

251 In cell divisions, relative size of daughter cells should play fundamental roles in gametoge

252 In contrast, the dispersion of daughter cell size depends on the forms of cell division

253 l Q.a daughter by promoting asymmetry in the daughter cell sizes of the Q.a neuroblast division but b

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

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

256 ges with each cell division and yet produces daughter cells that are largely rejuvenated, suggesting

257 result in neuroblast divisions that generate daughter cells that are more equivalent in size.

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

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

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

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

262 tor cells with binary potential give rise to daughter cells that have distinct functions.

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

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

265 d by their ability to self-renew and produce daughter cells that proliferate and mature.

266 Daughter cells that received fewer old mitochondria main

267 entify an asymmetry in pH between mother and daughter cells that underlies aging and rejuvenation.

268 This effect correlates with the survival of daughter cells that would normally die.

269 r cell to protect the functional capacity of daughter cells, the fate of ER protein aggregates is det

270 Before chromosomes segregate into daughter cells, they align at the mitotic spindle equato

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

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

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

274 ional coactivator SYS-1/beta-catenin between daughter cells to differentially activate Wnt-responsive

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

276 expressing Dl induce high Notch activity in daughter cells to promote EC formation.

277 through cell divisions is essential for the daughter cells to retain a proper cell identity.

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

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

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

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

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

283 g mother cells and limits lifespan, but that daughter cell vacuoles re-acidify.

284 Organelles are distributed to daughter cells, via inheritance pathways.

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

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

287 a loss of asymmetric size distribution among daughter cells when clpA is depleted from a strain in wh

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

289 it, which is inherited asymmetrically by one daughter cell, whereas the other one is born clean.

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

291 ence in T lymphocyte fates by giving rise to daughter cells with a propensity towards the terminally

292 lutionarily conserved process that generates daughter cells with different fates through the unequal

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

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

295 n in Bacillus subtilis creates unequal sized daughter cells with dissimilar programs of gene expressi

296 a broad range of cell types to generate two daughter cells with distinct cell fates.

297 asymmetrically, stem cells can generate two daughter cells with distinct fates.

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

299 hromosome segregation in anaphase by causing daughter cells with old centrosomes to retain non-disjoi

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