ライフサイエンスコーパス: morphological defect

1 an, sterility, uncoordinated locomotion, and morphological defects).

2 Addition of an M signal leads to gross morphological defects.

3 and indeed it may contribute to the observed morphological defects.

4 Fgf10 expression may contribute to the Dicer morphological defects.

5 y activity but did not result in any obvious morphological defects.

6 th in an animal model of cryptococcosis, and morphological defects.

7 ue to RNA interference also exhibited floral morphological defects.

8 f the mammalian Rb protein, cause no obvious morphological defects.

9 Longer germination revealed morphological defects.

10 The axr1 mutants display a variety of morphological defects.

11 in photoreceptor neurons results in striking morphological defects.

12 hich can bypass farnesylation, rescues these morphological defects.

13 ese immunopositive taste cells had apoptotic morphological defects.

14 l mutant to basic pH but did not correct the morphological defects.

15 st null animals die as late embryos with few morphological defects.

16 that is associated with DNA aberrations and morphological defects.

17 lack photoreceptor R7 alongside more complex morphological defects.

18 n are fertile, develop normally, and show no morphological defects.

19 e pole body duplication, exhibited lysis and morphological defects.

20 expressed in the limb leads to a variety of morphological defects.

21 C and 37 degrees C. rom2 delta cells exhibit morphological defects.

22 The presence of salt enhances these morphological defects.

23 f inhibitors of the ERK pathway reversed the morphological defects.

24 with no obvious cell swelling, twisting, or morphological defects.

25 rkin null mutants, do not show mitochondrial morphological defects.

26 plastid proteins, chmp1 plastids show severe morphological defects and aberrant division.

27 The Deltapch1 mutation causes pleiotropic morphological defects and an associated growth deficienc

28 2-deficient bradyzoite stages leads to gross morphological defects and complete ablation of cyst form

29 The morphological defects and decreased expression of ecdyso

30 xpressing HESO1 in hen1-2 causes more severe morphological defects and less accumulation of miRNAs.

31 The morphological defects and lethality were suppressed by m

32 e-aged CES rats, and then tested whether the morphological defects and poor memory performance in the

33 HDACi treatment rescued gross morphological defects and reduced CMZ cell death by 80%.

34 es with CSN reduced-function plants, such as morphological defects and reduced responses to auxin, ja

35 Depletion of bolA resulted in slow growth, morphological defects and the accumulation of high level

36 embrane binding sequence did not reverse the morphological defects and was lethal at low levels of ex

37 suppressed PINK1 RNAi-induced mitochondrial morphological defect, and overexpression of PINK1 or Par

38 ic ecdysteroid titers, severe late embryonic morphological defects, and a failure to induce IMP-E1.

39 synthesize enterobactin display no growth or morphological defects, and adding exogenous enterobactin

40 Early morphological defects appear to affect distribution of d

41 Accompanying these morphological defects are alterations in the expression

42 These morphological defects are associated with a profound fai

43 Morphological defects are first detected at E8.0 in the

44 These morphological defects are not detected in neurons that a

45 However, morphological defects are observed at the anterior end o

46 Morphological defects are observed in development of the

47 perfamily members are viable with only minor morphological defects, arguing for the existence of an a

48 ants identified hypotonia and behavioral and morphological defects as common features in addition to

49 Hair bundles show morphological defects as the mutant mice age and while m

50 Loss of these cables results in morphological defects as vesicles accumulate at the neck

51 GCS1 disruption strain (gcs1Delta) exhibited morphological defects, as well as mislocalization of cor

52 is a non-essential gene, and the sole overt morphological defect associated with null mutations in t

53 n, these low NtPSA1 plants displayed several morphological defects associated with auxin resistance s

54 e, whereas only Pbs2(AA) cells exhibited the morphological defects associated with loss of Hog1 funct

55 mitochondria in sporulating cultures reveals morphological defects associated with the loss of fusion

56 pamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4,

57 which are independent of sequence, result in morphological defects at later stages of development.

58 On the basis of the morphological defects at neuromuscular junctions, we pos

59 Various morphological defects at the neuromuscular junction in l

60 Loss of Rae1 function in neurons results in morphological defects at the neuromuscular junction that

61 s of embryonic ion channel function leads to morphological defects, but the underlying reason for the

62 ution revealed severe growth retardation and morphological defects by E8.5-E9.5.

63 Rescue of these morphological defects by exogenous auxin indicates a lin

64 Most significantly, we can rescue the morphological defects by re-introducing retinoic acid, o

65 Developmental and morphological defects caused by deletion of flbA encodin

66 These three alleles all reduced morphological defects caused by expression of the foreig

67 ies (AAA(+)), whose deletion causes a unique morphological defect characterized by the formation of k

68 tating forebrain abnormality with a range of morphological defects characterized by loss of midline t

69 Treated embryos were examined for gross morphological defects, ciliary function, and gene expres

70 x1-7 mutation acts to partially suppress the morphological defects conferred by the axr1-12 mutation.

71 wri null cells also have a morphological defect consistent with an increase in the

72 ion in explant culture, but instead produces morphological defects consistent with a role for Hh sign

73 acking yar RNAs are viable and show no overt morphological defects, consistent with maintained transc

74 These synaptic and morphological defects correlate with deficiencies in beh

75 rm in the oxidized one, due to cracks and/or morphological defects created during the oxidation proce

76 elop normally and do not have the pronounced morphological defects detected in cones.

77 We find that BCCIP depletion leads to morphological defects, disoriented mitotic spindles, chr

78 ble mutants nor the cmt3 single mutants show morphological defects, drm1 drm2 cmt3 triple mutant plan

79 phores and temporary paralysis, but no gross morphological defects during embryonic stages.

80 used by modulation of dopamine levels, while morphological defects during follicle formation likely r

81 This is accompanied by morphological defects, elevation of senescence-associate

82 effect on viability and produces no obvious morphological defects, except during oogenesis.

83 Despite the gross morphological defects, further analyses find no evidence

84 This was accompanied by SR morphological defects, impaired Ca(2+) release, and an a

85 ns, when deleted in mice results in a severe morphological defect in the rostral migratory stream and

86 Loss of Foxd1 causes a morphological defect in which the anterior lobe of the p

87 l YABBY gene activities have a wide range of morphological defects in all lateral organs as well as t

88 Morphological defects in chimeras included failure to fo

89 hymally, 3D reconstructions showed important morphological defects in epithelial tissues at the cap a

90 Morphological defects in Gata4/Gata6 mutant pancreata we

91 asmic microtubule network and display severe morphological defects in genetic backgrounds that produc

92 Perinatal lethality and morphological defects in homozygotes were rescued by die

93 Indeed, Cul3-depleted cells display severe morphological defects in LEs that could account for thes

94 MO25, increased lifespan and ameliorated all morphological defects in liver by postnatal day 21.

95 showed a 10-fold loss in viability and gross morphological defects in low oxygen conditions.

96 ss of Foxp2 results in increased severity of morphological defects in mutant lungs and leads to perin

97 localization of hr mRNA with the site of the morphological defects in mutant skin implicates hr as a

98 In this study, we report morphological defects in neurons and neuromuscular defec

99 mutant mice in the neonatal period exhibited morphological defects in organization and loss of hormon

100 In addition, morphological defects in other extraembryonic and embryo

101 However, we observed molecular and morphological defects in ovaries lacking beta-catenin, i

102 taneous intestinal inflammation, but exhibit morphological defects in Paneth and goblet cells.

103 a terminal web protein, but we see no gross morphological defects in the adult apical brush border i

104 ystogenic effect is associated with striking morphological defects in the cilia of Pkd1(-/-);Nedd9(-/

105 t conditional mutant mice show no detectable morphological defects in the cytoarchitecture of the bra

106 stering of junctional components, leading to morphological defects in the developing embryo.

107 Disruption of mouse Tulp3 results in morphological defects in the embryonic craniofacial regi

108 n, examining each of them histologically for morphological defects in the eye and behaviorally for ov

109 cup and stalk may underlie the molecular and morphological defects in the Foxg1(-/-) mutant.

110 stead, both ceh-28 and dbl-1 mutants exhibit morphological defects in the g1 gland cells located adja

111 z-1 function by RNA interference also caused morphological defects in the head or tail region of larv

112 simulations reveal that IL cations nucleate morphological defects in the microbial cell membrane at

113 n approximately 70% of neurons reversed many morphological defects in the motor cortex, including neu

114 ves from JAM-C SC KO mice were found to have morphological defects in the paranodal region, exhibitin

115 he cortical proliferative zone and there are morphological defects in the Pax6(Sey/Sey) (Pax6 null) c

116 kely to be captured by cationic vacancies or morphological defects in the real oxide, no charge trans

117 Therefore, one of the earliest detectable morphological defects in the SMA mice is the loss of syn

118 OD1 is sufficient to prevent biochemical and morphological defects in the Sod1(-/-) model, and to res

119 tion of peb-1 function using RNAi results in morphological defects in the somatic tissues in which pe

120 ed that loss of nhr-6 function causes severe morphological defects in the spermatheca and associated

121 t and spalt-related function in flies yields morphological defects in the testes, genitalia, and the

122 ESAM-/- mice did not show overt morphological defects in the vasculature.

123 Of the nine strongest, six have morphological defects in the ventral-type C (VC) neurons

124 flies with reduced DNAprim activity display morphological defects in their eyes, and unlike faf muta

125 acortical, excitation leads to axo-dendritic morphological defects in these interneurons.

126 Stereociliary morphological defects in USH2 mutant mice suggest roles

127 that hatchery-reared juveniles might exhibit morphological defects in vulnerable mechanosensory syste

128 CHS2 produced strains that showed no obvious morphological defects in yeast vegetative growth or in a

129 The morphological defects include an overall reduction in si

130 outer segment (OS) length, as well as gross morphological defects including hypopigmentation and per

131 c inflow tract that later displays prominent morphological defects, including a closed nonseptated he

132 , die around embryonic day 9.5 with multiple morphological defects, including abnormal folding of the

133 r viability, DeltadipM cells exhibited gross morphological defects, including cell widening and filam

134 nd cholinergic neurons display age-dependent morphological defects, including cytoskeletal disorganiz

135 ranule neurons lacking Trim9 exhibit several morphological defects, including excessive dendritic arb

136 Mutants of mldA or mldB had morphological defects, including loss of rod shape (a cu

137 and displayed growth retardation and certain morphological defects, including malformations of the ve

138 activity of a single TF resulted in specific morphological defects, including muscle targeting and de

139 tants are viable and fertile with only minor morphological defects, including the formation of an ect

140 These morphological defects indicate RlpA is needed for effici

141 fragment transplantation each yielded unique morphological defects indicating both epithelial and str

142 nd loss of this activity results in vacuolar morphological defects, indicating that PtdIns(3,5)P(2) i

143 s is that, with the exception of bldB, their morphological defect is carbon-source dependent.

144 The morphological defect is not observed in mutants for the

145 esult, Pebble-depleted adult flies exhibited morphological defects likely caused by cell death during

146 ts that eclose as adults display an array of morphological defects, many of which are shared by hep m

147 The morphological defects mimic those observed in humans and

148 cell wall integrity; and (3) exhibits marked morphological defects, most notably the accumulation of

149 In contrast, the only morphological defect observed in aux1 mutants is a loss

150 for stimulating translation and inducing the morphological defects observed by mRNA overexpression.

151 These findings suggest that the morphological defects observed in cul1-6 plants are caus

152 mutant peb-1(cu9) that not only exhibits the morphological defects observed in peb-1(RNAi) animals, b

153 Complementation of the morphological defect of bldA and bldB mutants with a clo

154 for Kir2.1 in BMP signaling may explain the morphological defects of Andersen-Tawil Syndrome and the

155 AtNOA1 leader peptide complements growth and morphological defects of Atnoa1 mutant plants.

156 However, the progressive hearing loss and morphological defects of hair cells in adult Pls1 KO mic

157 44A) effector domain mutant allele displayed morphological defects of highly elongated and multielong

158 cycle regulator Cdk1 play key roles in these morphological defects of isc1Delta cells.

159 mutant animals are viable and display subtle morphological defects of olfactory cilia only.

160 lly suppresses the cold-sensitive growth and morphological defects of S. pombe cells carrying a hypom

161 zebrafish leads to impeded bioenergetics and morphological defects of the heart and eyes.

162 The transcriptional and morphological defects of the mds3 Delta/Delta mutant wer

163 Here we demonstrate that morphological defects of the notochord in zebrafish can

164 Strikingly, p63 null mice show morphological defects of the organ of Corti, with supern

165 Adult mutants also show morphological defects of the vestibular apparatus, inclu

166 nd did not complement the protein sorting or morphological defects of the vps4 delta1 mutant.

167 phenotypes, including developmental arrest, morphological defects of the vulva and tail, and reduced

168 ete cytokinesis leading to embryo lethality, morphological defects, or multinucleate cells [2, 3].

169 resulting wdpks1Delta disruptants showed no morphological defects other than an albino phenotype and

170 Though a disc formed, it exhibited morphological defects, partial fusion with the glenoid b

171 phylococcus aureus exhibit severe growth and morphological defects, questioning whether these ftsZ mu

172 he A. fumigatus T6PP, OrlA, displayed severe morphological defects related to asexual reproduction wh

173 levels of WS5995B and displayed conditional morphological defects reminiscent of defects seen in Str

174 t rhodopsin trafficking and cytoskeletal and morphological defects resulting in retinal degeneration

175 A closer examination of the morphological defects revealed swollen hyphae, leaky tip

176 del of severe SMA, but not controls, display morphological defects that are consistent with a Z-disc

177 n in polar auxin transport, and a variety of morphological defects that can be ascribed to changes in

178 from Drosophila R7 photoreceptors causes two morphological defects that occur at distinct development

179 a detailed description of the age-dependent morphological defects that occur in identified neurons o

180 p or Prk1p caused a number of actin and cell morphological defects that were not observed when the ki

181 horylation sites exhibited severe growth and morphological defects that were partially reversed in a

182 In mutant embryos with the most severe morphological defects, the majority of tissue identities

183 Bmp signaling during this window results in morphological defects to the pouches and craniofacial sk

184 Consistent with the morphological defects, transgenic mice also have slower

185 le-gene disruptions did not show any obvious morphological defects under greenhouse conditions, where

186 Mechanistic insight into this morphological defect was obtained from a mouse mammary c

187 Based on the observed morphological defects, we named the two chromatin remode

188 By contrast, morphological defects were absent in cesa9 embryos, visu

189 At embryonic day 9 (E9) and beyond, morphological defects were apparent in the otic capsule

190 These morphological defects were correlated with altered expre

191 Homozygous mutants with morphological defects were first detected at E7.0 and we

192 These morphological defects were largely restricted to motor n

193 While no morphological defects were observed in Rac3(-/-) mice, R

194 albeit less striking, neuronal migration and morphological defects were observed on Zac1 knockdown, i

195 Importantly, splicing changes and morphological defects were rescued by expression of morp

196 Furthermore, the cdc42(V44A) morphological defects were suppressed by deletion of the

197 High-dose Lgi1a morphants have morphological defects which persist into adult stages th

198 including MRC1, TOF1, or CSM3 display basal morphological defects, which increase following HU treat

199 ve synapse formation and a variety of tissue morphological defects without detectably altering the ab