ライフサイエンスコーパス: growth defect

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

2 with human counterparts results in a severe growth defect.

3 tivation results in a hemoglobin utilization growth defect.

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

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

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

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

8 disease latency associated with plasma cell growth defect.

9 e addition of catalase partially rescued the growth defect.

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

11 Supplying Ile reversed the root growth defect.

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

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

14 notype arises, at least in part, from a cell growth defect.

15 o altered host immunity and not an intrinsic growth defect.

16 ered dendritic development, and marked spine growth defect.

17 rer2) complemented the temperature-sensitive growth defect.

18 esiculation was toxic and contributed to the growth defect.

19 ion of catalase in the medium alleviated the growth defect.

20 expression in chondrocytes showed a dramatic growth defect.

21 pairings, and a fifth displayed a synthetic growth defect.

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

23 esponsible for the reduced proliferation and growth defect.

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

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

26 h the mutant strain displaying a substantial growth defect.

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

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

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

34 lted in suppressor mutations that eliminated growth defects.

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

36 licating NADPH oxidase function in latd root growth defects.

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

38 ethylketones in their leaves but had serious growth defects.

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

40 Luminescent strains displayed no in vitro growth defects.

41 almost every amino acid substitution caused growth defects.

42 ltaDDD) displayed modest DNA replication and growth defects.

43 interact with Ura2 or rescue CPR6-dependent growth defects.

44 es, yet deletion strains display only subtle growth defects.

45 ective in the spindle checkpoint and exhibit growth defects.

46 verely compromised cell envelopes and strong growth defects.

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

48 kes it possible to identify subtle synthetic growth defects.

49 elevated lipid synthesis and subsequent hair growth defects.

50 is just accurate enough to avoid substantial growth defects.

51 adaptor proteins in ETI cells causes severe growth defects.

52 5-GFP and resulted in severe germination and growth defects.

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

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

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

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

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

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

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

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

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

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

63 tly suppress the postembryonic root meristem growth defect and the associated perturbed protophloem d

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

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

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

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

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

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

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

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

72 3 and SlCPTBP are required to complement the growth defects and dolichol deficiency of the yeast doli

73 is report, we found that the rrp1 mutant had growth defects and formed membrane blebs that led to cel

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

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

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

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

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

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

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

81 We also show that it detects growth-defect and growth-advantage genes previously show

82 er, while also allowing for the detection of growth-defect and growth-advantage regions.

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

84 aberrant levels of Pho regulon transcripts, growth defects, and changes in cell size and exopolysacc

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

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

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

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

89 These growth defects are also evident when this nuclease mutan

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

91 E4 mutant growth defects are substantially rescued in cells lackin

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

93 ver, the resulting vector displayed the same growth defect as the hexon-modified vector carrying all

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

95 of LVS clpB was not due to an intracellular growth defect, as LVS clpB grew similarly to LVS in prim

96 The growth defect associated with dPIP4K loss of function is

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 Ta-king advantage of the growth defect conferred by overexpressing SCT1, we ident

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

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

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

120 By contrast, this growth defect did not require the wzz(fepE) gene, which

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

122 ation in vivo and in ex vivo cultures, where growth defects due to lack of TIGAR were rescued by ROS

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

124 t 10 of 14 aneuploid yeast strains exhibit a growth defect during G1.

125 e mucR deletion strain exhibits a pronounced growth defect during in vitro cultivation and, more impo

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

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

128 We also report growth defects for two additional mutant strains (linc-B

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

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 ity to use non-haem iron sources in vitro, a growth defect in a low iron medium that is enhanced at p

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

134 se macrophages, the hcl1 mutant had a severe growth defect in BMDMs, indicating that HMG CoA lyase ge

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

136 Ad5 vectors displayed an approximate 10-fold growth defect in complementing cells, making potential v

137 -CSI3 cannot complement the anisotropic cell growth defect in csi1 mutants, suggesting that CSI3 is n

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

139 incidence of NTDs and partially rescues the growth defect in embryos lacking Mthfd1l.

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

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

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

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

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

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

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

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

148 RNAi-mediated ablation resulted in a growth defect in vitro and led to a sevenfold increase i

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

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

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

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

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

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

155 lomere shortening, fragility and fusion, and growth defects in culture.

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

157 is hypothesis: their inactivation results in growth defects in iron-chelated media, without affecting

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

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

160 Termination and growth defects in sen1 mutant cells are partially suppre

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

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

163 stimulates neurite growth and rescues axonal growth defects in SMN-deficient spinal cord neurons from

164 ter two exhibiting incomplete penetrance and growth defects in survivors.

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

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

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

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

169 e daughters' uterine environment, leading to growth defects in wild-type grandprogeny, and the appear

170 chbC in the mutant successfully rescued the growth defect, indicating a regulatory role of Rrp1 in c

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

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

173 The growth defect is likely due to a defect in capsid assemb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 and fructose-6-phosphate rescues the alphaMG growth defect of an sgrS mutant.

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

190 disruption ameliorating the cytokinetic and growth defect of DeltagcrA cells.

191 ents of these TonB systems to complement the growth defect of Escherichia coli W3110 mutants KP1344 (

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

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

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

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

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

197 The growth defect of S. aureus tagB and tarFJ mutants was al

198 The growth defect of the DeltalbtP mutant in macrophages is

199 WTA synthesis with tunicamycin, whereas the growth defect of the Deltalcp mutant was not relieved by

200 In addition, the observed growth defect of the DeltatofI strain, LSUPB145, was res

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

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

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

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

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

206 rologous complementation of the cold-induced growth defect of the yeast Deltarei1 deletion.

207 showed that the transporter complements the growth defect of the yeast fen2Delta pantothenate transp

208 t1g14560 and At4g26180) all complemented the growth defect of the yeast leu5Delta mitochondrial CoA c

209 naerobic conditions, while the intracellular growth defect of this strain could be complemented by th

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

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

212 utative plastid ADS3 paralog exacerbates the growth defects of ads2 mutant plants under low temperatu

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

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

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

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

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

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 of p85alpha and/or p85beta do not rescue the growth defects of p85alpha(-/-) cells, suggesting cooper

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

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 background could partially rescue the severe growth defects of the mutant.

225 -STUbLs) complemented to varying degrees the growth defects of the Schizosaccharomyces pombe STUbL mu

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

227 y activated miR408 is able to complement the growth defects of the T-DNA lines.

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

229 mutants are glycogen-deficient and exhibited growth defects on raffinose.

230 B had no detectable loss in viability and no growth defects or changes in spontaneous mutation freque

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

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

233 A growth defect phenotype was observed and genetically com

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

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

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

237 U0126 and PD325901 rescues the Npr2(pwe/pwe) growth defect, providing a promising foundation for skel

238 This growth defect required the PmrA-activated gene wzz(st),

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

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

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

242 persensitive to deferoxamine and displayed a growth defect similar to that observed following RNAi.

243 e CpgA protein present the morphological and growth defects similar to those of a cpgA-deleted strain

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

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

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

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

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

249 eltadegP strain displayed a high-temperature growth defect that corresponded to the production of few

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

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

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

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

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

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

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

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

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

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

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

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

262 PDH-deficient parasites have no blood-stage growth defect, they are unable to progress beyond the oo

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

264 in the mis-regulation of several genes and a growth defect under hypoxic conditions.

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

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

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

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

269 DeltahpnP mutant, however, did not exhibit a growth defect under the stress conditions tested except

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 ither subunit of the CBC confers a synthetic growth defect when combined with deletion of genes encod

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

289 members that disrupt H3K4 methylation have a growth defect when grown in the presence of the antifung

290 The DeltaEF2638 mutant also exhibited a growth defect when grown with aeration on several carbon

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

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

293 We show that there is a clear YchM-dependent growth defect when succinate is used as the sole carbon

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

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

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

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

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

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

300 synthesis of Fe-S clusters, led to synthetic growth defects with the crd1Delta mutant.