ライフサイエンスコーパス: growth defect

1 W1(Sec4) as the sole copy of YPT1 exhibit no growth defect.

2 esponsible for the reduced proliferation and growth defect.

3 gene (rpt2(E301K)) suppressed the ubi4Delta growth defect.

4 h the mutant strain displaying a substantial growth defect.

5 with human counterparts results in a severe growth defect.

6 tivation results in a hemoglobin utilization growth defect.

7 a dominant-negative phenotype with a severe growth defect.

8 henotype of the Kbtbd5 null mice but not the growth defect.

9 leads to reduction in lignin content but no growth defect.

10 ed by two-hybrid analysis, did not display a growth defect.

11 disease latency associated with plasma cell growth defect.

12 e addition of catalase partially rescued the growth defect.

13 A from the bacterial envelope and displays a growth defect.

14 Supplying Ile reversed the root growth defect.

15 e together responsible for the ssaB mutant's growth defect.

16 ine also suppressed the DspA/E-induced yeast growth defect.

17 absence of both proteins results in a strong growth defect.

18 s lacking the EEF1A ortholog showing a major growth defect.

19 mutation seen in our family led to a milder growth defect.

20 verely compromised cell envelopes and strong growth defects.

21 d-type strain and does not exhibit any major growth defects.

22 kes it possible to identify subtle synthetic growth defects.

23 elevated lipid synthesis and subsequent hair growth defects.

24 is just accurate enough to avoid substantial growth defects.

25 adaptor proteins in ETI cells causes severe growth defects.

26 5-GFP and resulted in severe germination and growth defects.

27 ructures accompanied by severe developmental growth defects.

28 acid to mga2Delta cells rescued the observed growth defects.

29 he hippocampus, as well as axon and dendrite growth defects.

30 n, while clrD, clrE and clrF had less severe growth defects.

31 -mediated genome instability leads to severe growth defects.

32 ltransferase (qua2-1 plants), display severe growth defects.

33 l cells correlated well with the severity of growth defects.

34 c death, loss of mTORC1 activity, and severe growth defects.

35 lted in suppressor mutations that eliminated growth defects.

36 e mutants, elicited severe dominant-negative growth defects.

37 licating NADPH oxidase function in latd root growth defects.

38 vated GAL1 and also produced mRNA export and growth defects.

39 ethylketones in their leaves but had serious growth defects.

40 chaeal strains exhibit temperature-dependent growth defects.

41 otential mechanism underlying the intestinal growth defects.

42 f Cdc5 with Cse4 at the kinetochore leads to growth defects.

43 leads to severe protein mislocalization and growth defects.

44 ion mutations result in severe intracellular growth defects.

45 lex leads to toxic levels of SigM and severe growth defects.

46 th in the double-mutant 2xuief caused modest growth defects.

47 ph1 during DNA damage stress results in cell growth defects.

48 lar protein production resources, leading to growth defects, a phenomenon known as the protein burden

49 or (CPF) subunits Ppn1 and Swd22 and elicits growth defects absent CPF subunits Ctf1 and Dis2 and ter

50 Notably, by screening cancer cell lines for growth defects after exposure to 5hmdC, we unexpectedly

51 nable to synthesize ppGpp display pronounced growth defects after exposure to darkness.

52 e loss of Hfq chaperone resulted in extended growth defect, alterations in the lipid A structure, mot

53 rter PLGG1 (bass6, plgg1) showed an additive growth defect, an increase in glycolate accumulation, an

54 nto selenoproteins, results in a significant growth defect and a global loss of selenium incorporatio

55 in budding yeast cells, we observed a severe growth defect and a substantially decreased DNA replicat

56 th genetic data, we suggest that the extreme growth defect and hyper-recombination phenotype of Top3-

57 te ER-ER fusion, but sey1Delta cells have no growth defect and only slightly perturbed ER structure.

58 A herA mutant exhibits an aerobic growth defect and reduced Por and Oor activities after e

59 genes tested (61%) could complement a lethal growth defect and replace their yeast orthologs with min

60 Iron supplementation reversed this growth defect and was associated with FBXL5-dependent po

61 erminal Fe4 S4 cluster in vitro, caused mild growth defects and a significant decrease in the activit

62 SN3 deletion mutant had a nutrient-dependent growth defects and abnormal conidium morphology.

63 in the ubiquitin-binding site of Dss1 cause growth defects and accumulation of ubiquitylated protein

64 A DeltaUL46 virus displayed growth defects and activated innate immunity, but both e

65 eated with 3-hydroxyoctanoate have ech2-like growth defects and altered IBA responses.

66 mus81 and tdp1 mus81 double mutants exhibit growth defects and an increase in dead cells in root mer

67 ir cerebral anomalies, which result in brain growth defects and cognitive dysfunction.

68 An axy9 insertional mutant exhibits severe growth defects and collapsed xylem, demonstrating the im

69 logical Reep1 mutations resulted in neuritic growth defects and degeneration.

70 3 and SlCPTBP are required to complement the growth defects and dolichol deficiency of the yeast doli

71 ckdown of matrilin-1 results both in overall growth defects and in disturbances in the formation of t

72 The Fgpal1 mutant had severe growth defects and often displayed abnormal hyphal tips.

73 3 wk after birth with signs of both general growth defects and potential cerebellum-related neuronal

74 Because hypothyroidism leads to growth defects and premature death in mice, we assayed f

75 Furthermore, sdeA and gcsA mutants displayed growth defects and raft mislocalization, which were acco

76 d rud3Delta) caused strong glycosylation and growth defects and reduced membrane association of the C

77 of a peptide containing this sequence causes growth defects and sensitizes Escherichia coli to antibi

78 nd the GET system exhibit strong synergistic growth defects and severe mitochondrial damage, includin

79 result in a weak mutator phenotype and cause growth defects and synergistic increases in GCR rates wh

80 mutants, cen10Delta mutant strains exhibited growth defects and were aneuploid for chromosome 10.

81 f each of the genes results in a significant growth defect, and that each protein catalyzes a unique

82 c phenotypes, including early-onset obesity, growth defects, and metabolic dysregulation.

83 hTERT-P785L-expressing cells did not show growth defects, and this variant likely confers cell sur

84 educe MT stability, and cause severe neurite growth defects; and 3) neomorphic mutations, which map t

85 This growth defect appears to be linked to the suppression of

86 wise, depletion of nutrients exacerbated the growth defect ( approximately 56%), which was partially

87 Growth defects are most pronounced when S. aureus is cul

88 The mutant has no growth defect, arguing against ongoing restriction of it

89 We also show that the lack of larval growth defects as well as nearly normal fatty acid compo

90 ubiquitin stabilizes Kog1 and suppresses the growth defect associated with the tor2 mutant at the non

91 We also found that many of the metabolic and growth defects associated with mutations in the trehalos

92 M MTB model, and it can successfully predict growth defects associated with TF overexpression.

93 n), we targeted and debugged the origin of a growth defect at 37 degrees C in glycerol medium, which

94 interference results in an O. tsutsugamushi growth defect at 72 h that can be rescued by amino acid

95 type, deletion of the loop as well generated growth defects at 37 degrees C, whereas the deletion of

96 s were sensitive to a range of drugs and had growth defects at low temperature.

97 ons in its ATP-binding Walker motifs exhibit growth defects at low temperatures.

98 P4 was knocked down or disrupted exhibited a growth defect, attributable to reduced viability of extr

99 nd the Arabidopsis GRXS15 able to complement growth defects based on disturbed ISC protein assembly o

100 growth under intermittent light, with severe growth defects being observed in a mutant lacking PTOX2,

101 Minor growth defect "bugs" detected in synXII, caused by delet

102 The Fgprp4 deletion mutant had severe growth defects but often produced spontaneous suppressor

103 ype Pol-gamma suppresses mutation-associated growth defects, but continuous growth eventually leads t

104 Reduction of CCT4 results in growth defects by affecting both cell size and prolifera

105 required for the suppression of fcp1 mutant growth defects by loss of CDK8 under oxidative stress co

106 x 1 (TORC1) effector NPR1 improves hal4 hal5 growth defects by stabilizing nutrient permeases at the

107 ple-negative breast cancer (TNBC), and these growth defects can be rescued with exogenous WT MELK, bu

108 S. mutans SRP pathway mutants demonstrate growth defects, cannot contend with environmental stress

109 f interacting environmental factors, the Mnp growth defect caused by Msx1 deficiency is modified by a

110 n defective (AMD) mutant of Scd6 rescues the growth defect caused by overexpression of Scd6, a featur

111 es of RPB9 in yeast that suppress the severe growth defect caused by rpb1-G730D, a substitution withi

112 ocompromised animals, albeit with a 400-fold growth defect compared with the growth of wild-type viru

113 rease in Mg(2+) content and displayed severe growth defects compared with single mutants alr1Delta an

114 mcm5-bob1 bypasses the growth defect conferred by DDK-phosphodead Mcm2 in buddi

115 that multiple mechanisms contribute to cell growth defects conferred by the IFD variants.

116 RTEL1 suppressed the telomere shortening and growth defect, confirming the causal role of the RTEL1 m

117 cking both Hrd1 and Ste24 exhibit a profound growth defect, consistent with overlapping function.

118 the nos srrAB double mutant, and its aerobic growth defect could be partially rescued with supplement

119 The synthetic Vma(-) growth defect could not be attributed to loss of vacuola

120 The SPG3A axon growth defects could be rescued with microtubule-binding

121 ping or isthmus peristalsis rates, but their growth defect depends on the bacterial diet.

122 onocytogenes show severe lysis, division and growth defects due to distortions of cell wall biosynthe

123 e ectopic heterochromatin, leading to severe growth defects due to the inactivation of essential gene

124 r methylglyoxal, and carbon source-dependent growth defects, especially when grown on glycerol.

125 dD double mutant exhibits an almost complete growth defect, even in the absence of stress.

126 porters abrogates Ca(2+)- and Mn(2+)-induced growth defects, excessive Mn(2+) accumulation in the cel

127 identical to the previously identified CELL GROWTH DEFECT FACTOR 1 (CDF1) in Arabidopsis that is con

128 Growth defects from knockdown of 14-3-3 and Tctp are sup

129 as central to attenuation in vivo, whereas a growth defect imparted by the lipA mutation made a negli

130 genously added metabolites partially rescued growth defects imposed by QSSM synthesis.

131 We show that DDX3X complements the growth defect in a ded1 temperature-sensitive strain of

132 partially rescued the temperature-dependent growth defect in arv1Delta yeast, while p.(Lys59-Asn98de

133 permease gene scfD resulted in a monoculture growth defect in CDM that could be rescued by addition o

134 This growth defect in cells lacking Pex36 can be rescued by t

135 The DeltasbnD mutant, in contrast, showed no growth defect in either abscesses or epithelial cells.

136 Deletion of lepA confers no obvious growth defect in Escherichia coli, and the physiological

137 the TcVSP-OE parasites showed a significant growth defect in fibroblasts, less responsiveness to hyp

138 e in G. mellonella hemolymph, and also had a growth defect in human serum.

139 The selD CRISPR deletion mutant had a growth defect in protein-rich medium and mimicked the ph

140 visiae cho1Delta mutant rescued the mutant's growth defect in the absence of ethanolamine supplementa

141 A P3 mutant (DeltaP3) had a growth defect in the dark and a pigment defect that was

142 iMet binding to eIF2 in vivo and rescued the growth defect in the eIF2gamma-I318M strain.

143 A growth defect in the glycolysis-impaired mutant is cause

144 e reductase (napA mutant) exhibited a marked growth defect in the lumen of the colon.

145 re overflow metabolism), as well as a strong growth defect in the presence of acetate as sole carbon

146 We observed a strong growth defect in the presence of methionine.

147 escue telomere aggregation and the synthetic growth defect in this context, suggesting that SLX4IP fa

148 a VZV laboratory strain with no discernible growth defect in tissue culture, contained a 2,158-bp de

149 The deletion virus had a marked growth defect in vitro and could not be passaged in cult

150 Nine PKs had a more pronounced growth defect in vivo, than in vitro.

151 ila Cdc7 and Chiffon is able to complement a growth defect in yeast containing a temperature-sensitiv

152 osome core, as its depletion causes a severe growth defect in yeast.

153 s of Zap1-dependent UBI4 expression caused a growth defect in zinc-deficient conditions.

154 presses or enhances physical interaction and growth defects in an allele-specific manner, signifying

155 e plasma membrane, rescued secretion and bud growth defects in boi mutant cells, and abrogated NoCut

156 tream of Unpaired partially rescues the disk growth defects in Ipk2 mutants.

157 on pathway of E2 subunits is blocked, showed growth defects in minimal media even when supplemented w

158 M. tuberculosis strains lacking Rv1422 have growth defects in minimal medium containing limiting amo

159 s; however, these variants tended to exhibit growth defects in other environments.

160 r data also showed that the mutant displayed growth defects in regular BSK-II medium.

161 map genes that enhance or suppress growth defects in response to different mitochondrial in

162 To et al. map genes that enhance or suppress growth defects in response to different mitochondrial in

163 and pharmacologic modification of root hair growth defects in rhd3 suggest that there is interplay b

164 he P2-excised strain completely restores the growth defects in seawater medium and partially restores

165 t is inducing changes in auxin transport and growth defects in shoot tissues.

166 of AKR1C3 partially rescued AR activity and growth defects in Siah2 knockdown cells, suggesting a no

167 r, Rad53 deficiency causes histone-dependent growth defects in the absence of DNA damage, pointing ou

168 We then use u-CT imaging to study growth defects in the Drosophila brain through the chara

169 iae GAL coding regions gave rise to profound growth defects in the S. bayanus background.

170 KCvarepsilon in a TNBC cell model results in growth defects in two-dimensional (2D) and three-dimensi

171 t resulted in increased basal p53 levels and growth defects in vitro and in vivo Consistent with thes

172 cyte cultures from patients with CHH display growth defects in vitro, which is consistent with an imm

173 nsitivity in remodelling and leads to severe growth defects in vivo.

174 Expression of CinA also rescues CinB-induced growth defects in yeast.

175 d prolamine RNAs and conferred other general growth defects, including dwarfism, late flowering, and

176 ble mutant rtel1-1 recq4A-4 exhibits massive growth defects, indicating that this RecQ family helicas

177 Mutation of FgVPS35 not only mimicked growth defects induced by pharmacological treatment, but

178 Here, we show that cell growth defect is likely explained primarily by slow Ribo

179 media lacking aromatic amino acids, and the growth defect is rescued by inclusion of the aromatic am

180 This intracellular growth defect is rescued only by the addition of excess

181 ys pollen germination and causes pollen tube growth defects, leading to drastically reduced fertility

182 cell death, and rice seedlings showed severe growth defects, leaf chlorosis and leaf shrinkage.

183 - and hTERT-R811C-expressing cells exhibited growth defects likely due to impaired TPP1-mediated recr

184 rge region bearing complex amplifications, a growth defect mapping to a recoded sequence in FIP1, and

185 the results presented here suggest that this growth defect may be due in part to misfolded FtsN.

186 are common events in cancer, this synthetic growth defect mediated by DAXX suppression represents a

187 glt1-knock-out parasites exhibited a growth defect not rescued by catalytically inactive Glt1

188 e conditions is highlighted by the synthetic growth defect observed between dun1Delta and fet3Delta f

189 However, the growth defect observed by expressing mcm10-m2,3,4 is not

190 by oxidative phosphorylation phenocopied the growth defect observed in the RsbU null strain.

191 ich caused synthetic enhancement of the root growth defects observed in a MAP kinase 4 (MPK4) single-

192 , suggesting that AtPRX71 contributes to the growth defects observed in plants undergoing cell wall d

193 Disruption of pntA resulted in phenotypic growth defects observed under low light intensities in t

194 ary for complementation of the intracellular growth defect of a DeltasidJ mutant.

195 (Ss)RidA-1 and (Ss)RidA-2 complemented the growth defect of a Salmonella enterica ridA mutant, an i

196 cues the cell cycle entry defect but not the growth defect of DCAF1-deficient cells.

197 The growth defect of Glx3-deficient cells in glycerol is als

198 nockout of GA2ox2 partially rescues the root growth defect of hdt1,2i These results suggest that by r

199 und is able to suppress the gravitropic root growth defect of hy5 mutants.

200 use fibroblasts and of WT KRAS to rescue the growth defect of mouse embryonic fibroblasts deficient i

201 Importantly, we showed that the growth defect of pUL92-deficient HCMV could be rescued i

202 The growth defect of the DeltalbtP mutant in macrophages is

203 arboxymycobactin did not rescue the low-iron growth defect of the export mutant but severely impaired

204 d we show here that Msx1 deficiency causes a growth defect of the medial nasal process (Mnp) in mouse

205 omoter in single copy was able to rescue the growth defect of the mutant.

206 An in vitro growth defect of the NMB0419 mutant under iron restricti

207 The growth defect of the pme6-1 mutant is rescued by maintai

208 The temperature-dependent growth defect of the sec3-913 strain was gene dosage-dep

209 After correcting this mutation, the growth defect of TX6051 was abolished, implicating a rol

210 N6390 strain, the DeltasfaA mutant exhibited growth defects of 2.2-fold.

211 STV1 overexpression suppressed the growth defects of both rav1 and rav1vph1, and allowed RA

212 nsive cell wall-related genes and the severe growth defects of BR mutants.

213 r named mongoose1 (mon1) that suppressed the growth defects of cobra, partially restored cellulose le

214 together with the coreceptor AtGET1 rescues growth defects of Deltaget1get2 yeast.

215 in the reference K-12 strain to compute the growth defects of each strain.

216 he dph1Delta and dph3Delta deletions rescued growth defects of elp3Delta in response to thiabendazole

217 ecific protein, FgSad1, which suppressed the growth defects of Fgprp4.

218 ted knockout strains to confirm the expected growth defects of GBS deficient in capsule or stringent

219 Hair growth defects of homozygous toku mice were partially re

220 uppressed the increased GCR rates and/or the growth defects of rnh203Delta double mutants.

221 Growth defects of the double mutants could be eliminated

222 nd stress conditions and can rescue the root growth defects of the Medicago truncatula lateral root-o

223 d7 intron 2, the complex I activity, and the growth defects of the mutant.

224 Consecutive deletions, resulting in growth defects of the skull and long bones, showed that

225 span of the pah1Delta mutant along with its growth defect on non-fermentable carbon sources and hype

226 get of AvrPto, AvrPtoB and HopF2, the strong growth defects or lethality associated with ectopic expr

227 lity to divide asymmetrically, nor show cell-growth defects or undergo apoptosis.

228 A growth defect phenotype was observed and genetically com

229 MTBPROM2.0 improves performance of knockout growth defect predictions compared to the original PROM

230 ease is less well understood with only minor growth defects previously reported for DeltaclpA cells.

231 BP and cause auxin resistance and associated growth defects, probably by protecting TIR1 substrates f

232 hat either K113E or E195K induces yeast cell growth defects rescued by E/K.

233 to inhibit liver cancer cell growth, and the growth defect resulting from loss of CaMKK2 can be rescu

234 lator crumbs, exhibiting varying rhabdomeric growth defects, revealed a correlation between increased

235 This indicates that the strong growth defects seen for plants lacking complex I origina

236 he expense of polysomes, suggesting that the growth defect stems from a shutdown of translation.

237 with znuABC mutants displaying a more severe growth defect, suggesting that both ZnuABC and ZrgABCDE

238 n a receptor knockout (KO) results in severe growth defects, suggesting presence of alternative inser

239 ability partially suppresses the pollen tube growth defects, suggesting that LRX proteins influence C

240 ompound in ref8 did not relieve the mutant's growth defects, suggesting that the hyperaccumulation of

241 th LDH and G3P dehydrogenase (GPDH1) exhibit growth defects, synthetic lethality and decreased glycol

242 in more severe morphological and respiratory growth defects than deletion of single MICOS subunits or

243 at: (i) bacteria making certain QSSMs have a growth defect that exerts an evolutionary cost, (ii) pro

244 y DinG is essential results in a significant growth defect that is rescued by complementation with En

245 The DacA null mutant presented a growth defect that manifested through an increased lag t

246 sidM lspF double mutant had an intracellular growth defect that was more dramatic than that of the ls

247 e SARS-CoV M chimera exhibited a conditional growth defect that was partially suppressed by mutations

248 lone expressing FabI(Y147H) had a pronounced growth defect that was rescued by exogenous fatty acid s

249 t it has a decreased rate of endocytosis and growth defects that are shared with other chc1 mutant al

250 tectable xyloglucan are viable, they display growth defects that are suggestive of alterations in wal

251 Two of these alleles display growth defects that can be strongly suppressed by overex

252 tii DeltapmrA exhibited severe intracellular growth defects that coincided with failed secretion of e

253 however, these mice showed severe postnatal growth defects that include an approximately 50% reducti

254 a major challenge owing to the occurrence of growth defects that result in poor materials behaviour i

255 ured either aerobically or anaerobically had growth defects that were alleviated by the addition of e

256 ble mutant combinations showed no observable growth defect, the mtacp1 mtacp2 double mutant was viabl

257 of TFIISmut in tfIIs plants provoked severe growth defects, transcriptomic changes and massive, tran

258 all four systems (null mutant) had a severe growth defect under aerobic conditions but accumulated i

259 ts of the pupylation machinery show a strong growth defect under iron limitation, which was caused by

260 visiae cells exhibit a temperature-sensitive growth defect under oxidative growth conditions and prod

261 The DeltakdpE mutant showed a significant growth defect under potassium-limited conditions and in

262 A ybtPQ-null mutant exhibited no growth defect under standard culture conditions, consist

263 the absence of mga2, fission yeast exhibited growth defects under both normoxia and low oxygen condit

264 function of CaWss1 in the suppression of the growth defects under DPC-inducing conditions.

265 t-negative phenotype that causes more severe growth defects under these same stress conditions.

266 In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primar

267 The iutA2 mutant shows growth defects upon iron limitation, alterations in Fe-s

268 logs, assaying for complementation of lethal growth defects upon loss of the yeast genes.

269 cells, respiratory chain inhibition leads to growth defects upon serine withdrawal that are rescuable

270 ntial apoptosis along with proliferative and growth defects upon the loss of Fbw7.

271 interaction in vitro and for pronounced cell growth defects upon translation inhibition in vivo, cons

272 To determine whether the growth defect was a result of loss of nuclease activity

273 The RNAi-induced growth defect was complemented by expression of wild-typ

274 tyostelium discoideum, and the intracellular growth defect was complemented by the phytase gene.

275 Interestingly, the mutant's growth defect was exacerbated in macrophages that had be

276 The pabA growth defect was found to be due to a combination of lo

277 No in vitro growth defect was observed for the Deltabb0318 clone.

278 Although no growth defect was observed for the mutant in normal BSK-

279 A severe growth defect was observed in the cshA mutant compared w

280 The pabA growth defect was specific to the red blood cell compone

281 M. tuberculosis Rv3780 mutant had a general growth defect, was sensitive to heat stress, and was att

282 long term survival experiments, significant growth defects were found in DeltaclsA strains and the D

283 These growth defects were not alleviated by either auxin treat

284 These observed growth defects were not the consequence of lignin pertur

285 Although no growth defects were observed, co- and post-translational

286 hese mutants exhibit a significant synthetic growth defect when combined with deletion of Hog1, a kin

287 hibit a full, temperature-independent Vma(-) growth defect when combined with the rav1 mutation.

288 mutant msn2Deltamsn4Delta exhibited a severe growth defect when grown with oleic acid as the sole car

289 es identified by this approach resulted in a growth defect when introduced into yeast.

290 The mutant displayed growth defects when cultured in vitro and resistance to

291 Moreover, cells display severe growth defects when elevated temperatures, amino acid an

292 tantly, CPCT-null parasites exhibited severe growth defects when ethanolamine and exogenous lipids be

293 We observed aberrant cell shape and severe growth defects when PknA was depleted.

294 An RsbU null mutant showed severe growth defects which could be restored through genetic c

295 osynthetic and receptor mutants have similar growth defects, which initially led to the assumption th

296 6 (IFI16); (iii) a DeltaUL46 virus displayed growth defects, which were rescued in STING knockdown ce

297 ential for aerobic growth exhibited a severe growth defect with an anode (+0.4 V(SHE)) or Fe(III)-NTA

298 in chondrocytes causes severe kyphosis and a growth defect with decreased chondrocyte proliferation,

299 tations of RAD53 and DUN1 caused a synthetic growth defect with sgs1Delta and elevated gross chromoso

300 a1 thioredoxin peroxidase caused a synthetic growth defect with the pah1Delta mutation.