ライフサイエンスコーパス: hypodermal

1 tein products of all three genes localize to hypodermal adherens junctions in embryos.

2 rmal and dermal thickness and an increase in hypodermal adipose tissue.

3 ion and quantification method for infectious hypodermal and hematopoietic necrosis virus (IHHNV), a s

4 g, we found that PEB-1 was detectable in all hypodermal and hindgut cells underlying the cuticle.

5 berrant expression of SKN-1 causes a loss of hypodermal and neuronal tissue and an excess of pharynge

6 Dysregulation of let-7 results in irregular hypodermal and vulval development.

7 cones extend fingers dorsally between these hypodermal attachment structures.

8 duced in size by different proportions, with hypodermal blast cell size most closely proportional to

9 the inappropriate deaths of many of the Pn.p hypodermal blast cells and prevent the surviving Pn.p ce

10 patterns were observed, either intestinal or hypodermal, but no gross RNAi phenotypes were found poss

11 al ovule development in maize, only a single hypodermal cell develops into an archesporial cell and t

12 shown that ELT-3 is not essential for either hypodermal cell differentiation or the viability of the

13 of ELT-1 in a redundant pathway controlling hypodermal cell differentiation.

14 In a normal anther a hypodermal cell divides periclinally with the inner cell

15 ot suppress defects in two different ventral hypodermal cell fate decisions in hermaphrodites and mal

16 In angiosperm ovules and anthers, the hypodermal cell layer provides the progenitors of meiocy

17 atory element which is sufficient to specify hypodermal cell reporter gene expression.

18 er transcription factor that is required for hypodermal cell terminal differentiation and proper vulv

19 he heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the fina

20 which formed regularly spaced stripes on the hypodermal cell.

21 and is essential for the production of most hypodermal cells (22).

22 The gene is expressed in hypodermal cells 4 hours before ecdysis during all larva

23 Abnormal organization of hypodermal cells and expression of a hypodermal marker i

24 he mutants had abnormal-shaped epidermal and hypodermal cells and showed an unusual arrangement of sm

25 ect the failure of mac1 gene function in the hypodermal cells and their cellular progeny.

26 in transgene is expressed in lateral rows of hypodermal cells and these cells fail to properly change

27 in the adult stage with strong expression in hypodermal cells and weaker expression in gut cells.

28 nt bundles at the adherens junctions between hypodermal cells and, thereby, transmit the force of bun

29 Mesodermal, endodermal, and hypodermal cells appear to be completely absent in most

30 endently of immediately adjacent neighboring hypodermal cells because dorsal intercalation is not blo

31 how that lin-26 is expressed not only in all hypodermal cells but also in all glial-like cells.

32 pecify and/or maintain the fates not only of hypodermal cells but also of all other non-neuronal ecto

33 This pathway is activated in hypodermal cells by the LET-23 epidermal growth factor r

34 In mac1 mutant ovules several hypodermal cells develop into archesporial cells, and th

35 ecifically in the nuclei of a variety of non-hypodermal cells during development.

36 elt-3 is expressed in all of the major hypodermal cells except the lateral seam cells, and expr

37 The external hypodermal cells fail to spread over and enclose the emb

38 plays an important role in the switch of the hypodermal cells from the vegetative pathway to the meio

39 plays an important role in the switch of the hypodermal cells from the vegetative to the meiotic (spo

40 les, LECT-2 decorates neuronal processes and hypodermal cells in a pattern similar to the cell adhesi

41 is the interactions of body wall muscle and hypodermal cells in Caenorhabditis elegans.

42 eir direction of migration; posterior dorsal hypodermal cells in die-1(w34) mutants appear to extend

43 The most posterior hypodermal cells in the tail define a specialized, sexua

44 aphrodites at the L2 stage there are 11 Pn.p hypodermal cells in the ventral midline arrayed along th

45 o drive expression of a seam marker in other hypodermal cells in wild-type animals, and in anterior h

46 est a model in which postembryonic growth of hypodermal cells is regulated by TGFbeta-related signali

47 The cpz-1 gene is expressed in various hypodermal cells of all developmental stages and is spec

48 Dorsal hypodermal cells of die-1(w34) homozygous embryos initia

49 ed exclusively in the intestine, seam cells, hypodermal cells of the main body syncytium, and the exc

50 utation alters the developmental fate of the hypodermal cells of the maize anther.

51 cZ) is widely expressed in the intestine and hypodermal cells of transgenic worms, while the fusion p

52 e progenitors for either half of the lateral hypodermal cells or the posterior half of the dorsal hyp

53 is and intestine, and expression of OSR-1 in hypodermal cells rescues the osr-1(rm1) phenotypes.

54 finger transcription factor, is required for hypodermal cells to acquire their proper fates.

55 ositional cues from muscle are transduced to hypodermal cells to direct sensory dendrite outgrowth.

56 Ce-Duox1 is expressed in hypodermal cells underlying the cuticle of larval animal

57 ed in late embryos and L2d predauers, in the hypodermal cells which synthesize the cuticle.

58 First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or

59 ls (including various muscle, intestinal and hypodermal cells) in high-resolution images of adult C.e

60 elongate properly, abnormal contacts between hypodermal cells, and failure of the pharynx to attach t

61 EGL-15 indicate that EGL-15 is expressed in hypodermal cells, and hypodermal promoters can drive ful

62 These cells, the hypodermal cells, either directly or indirectly form the

63 les in the intercalation of posterior dorsal hypodermal cells, in muscle cell positioning and in inte

64 eporter, which is localized to boundaries of hypodermal cells, shows that hypodermis is disorganized

65 neurons, the posterior intestine cells, tail hypodermal cells, the T cells and specific T-cell descen

66 d the dense body to the hemidesmosome on the hypodermal cells, which in turn instructed the SAX-7 str

67 ed could be due to improper specification of hypodermal cells.

68 r these genes in the function of the lateral hypodermal cells.

69 Weak expression is also detected in hypodermal cells.

70 threads formed, they aborted in epidermal or hypodermal cells.

71 in approximately 85 muscle, epithelial, and hypodermal cells.

72 nction of a wide range of nerve, muscle, and hypodermal cells.

73 MS lineage, a lineage that does not generate hypodermal cells.

74 nic genes in some, but not all, of these non-hypodermal cells.

75 solateral protrusions in distinct subsets of hypodermal cells.

76 drive reporter gene expression in posterior hypodermal cells.

77 ed EFF-1 alters the normal pattern of fusing hypodermal cells.

78 s been shown to pattern posterior muscle and hypodermal cells.

79 This enhancer drives GFP expression in hypodermal cells.

80 s, forming two longitudinal ribbons over the hypodermal cells.

81 ormed disorganized elastic fibers throughout hypodermal connective tissue as they aged.

82 The increased elastic fibers in Tsk hypodermal connective tissue was associated with increas

83 nesis associated with increased fibulin-2 in hypodermal connective tissues and decreased fibulin-5 at

84 y altering matrix protein composition in Tsk hypodermal connective tissues.

85 esting this gene is required for maintaining hypodermal-cuticle attachment as the animal grows in siz

86 the head cells and spermatheca is constant, hypodermal daf-9::GFP expression is modulated by multipl

87 ression pattern suggests a role for ELT-3 in hypodermal development, no functional studies have yet b

88 ryonic blastomeres, to activate a program of hypodermal differentiation even in blastomeres that are

89 opment and disrupts embryonic proliferation, hypodermal enclosure, and elongation.

90 Defects in late gastrulation, ventral hypodermal enclosure, and formation of the rectum result

91 em rescues a daf-5 mutant, whereas muscle or hypodermal expression does not.

92 ssue-specific promoter studies indicate that hypodermal expression of ptc-3 is required for normal de

93 ent protein gene (gfp) and demonstrated that hypodermal expression of the fusion gene is adult-specif

94 , a GATA transcription factor that specifies hypodermal fate in the embryo, as a regulator of sperm-s

95 way is not activated adopts a differentiated hypodermal fate.

96 cells in wild-type animals, and in anterior hypodermal-fated daughters in a Wnt pathway-sensitized b

97 -1 structure from mutant Tsk fibrillin cause hypodermal fibrosis and associated changes in dermal gen

98 between the muscle contractile apparatus and hypodermal fibrous organelles.

99 t the conclusion that mup-4 is essential for hypodermal function and that this function is necessary

100 ealed a previously unknown role for mab-9 in hypodermal function and we suggest that MAB-9 is require

101 We showed that ELT-3 can activate hypodermal gene expression in the absence of ELT-1 and t

102 T-1 and that, conversely, ELT-1 can activate hypodermal gene expression in the absence of ELT-3.

103 ithin the mantle, instead of the specialised hypodermal glands in the second antennular segment as re

104 In C. elegans, assembly of hypodermal hemidesmosome-like structures called fibrous

105 MUA-3 localizes to the hypodermal hemidesmosomes and to other sites of mechanic

106 e presumptive mua-6 null allele localizes to hypodermal hemidesmosomes.

107 Dermal and hypodermal hemorrhage is detected in mutant embryos at l

108 izations reveal that mutants have defects in hypodermal integrity and morphology.

109 ctive tissues and decreased fibulin-5 at the hypodermal M-CT interface suggest that these proteins me

110 tion of hypodermal cells and expression of a hypodermal marker in hbl-1(RNAi) animals suggests that m

111 utants, cell migrations are defective during hypodermal morphogenesis, QL neuroblast migration, and t

112 mup-4 is essential in embryonic epithelial (hypodermal) morphogenesis and maintenance of muscle posi

113 ayer found normally at the interface between hypodermal muscle and connective tissue was absent from

114 ion, and, at high levels, completely blocked hypodermal muscle contraction.

115 The lack of elastic fibers at the hypodermal muscle-connective tissue (M-CT) interface was

116 DIE-1 is present in the nuclei of hypodermal, muscle, gut, and pharyngeal cells; its distr

117 ntrast and fluorescence imaging of embryonic hypodermal nuclear migration events were used to charact

118 LIN-29 accumulates in all hypodermal nuclei during the L4 stage.

119 enesis of the Caenorhabditis elegans embryo, hypodermal (or epidermal) cells migrate to enclose the e

120 with an essential role of mag-1 in embryonic hypodermal organization and elongation.

121 e results in a severe defect in migration of hypodermal P cells to a ventral position.

122 C. elegans hypodermal P-cell larval nuclei traverse a narrow space

123 In Caenorhabditis elegans larvae, failure of hypodermal P-cell nuclear migration results in uncoordin

124 form the hermaphrodite vulva, a specialized hypodermal passageway used for egg laying and sperm entr

125 , resulting in a deformed vulva, and the P12 hypodermal precursor often differentiates into a second

126 erentiation even in blastomeres that are not hypodermal precursors in wild-type embryos.

127 EGL-15 is expressed in hypodermal cells, and hypodermal promoters can drive full clr-1 and egl-15 res

128 Mutations in mua-6 result in hypodermal rupture, muscle detachment from the bodywall,

129 suggesting that puf-9 and let-7 may mediate hypodermal seam cell differentiation by regulating commo

130 obust stage specificity of cell fates in the hypodermal seam cell lineages.

131 ls that express pal-1 and in the neighboring hypodermal seam cell precursors, which do not, as well a

132 28, and lin-29 specify the timing of lateral hypodermal seam cell terminal differentiation in Caenorh

133 results in ectopic Ptbx-2::gfp expression in hypodermal seam cells and gut.

134 l tip cell (DTC), intestine, and the lateral hypodermal seam cells but not in the main body hypoderma

135 the terminal differentiation of the lateral hypodermal seam cells during the larval-to-adult molt.

136 We find that OSM-11 is secreted from hypodermal seam cells into the pseudocoelomic body cavit

137 NCX-9 functions in hypodermal seam cells that secrete the axon guidance cue

138 upregulated during the last larval stage in hypodermal seam cells which is transcriptionally regulat

139 lutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-t

140 the Golgi apparatus occurring exclusively in hypodermal seam cells, pharyngeal cells, and spermatheca

141 nes are expressed exclusively in the lateral hypodermal (seam) cells.

142 proliferation of the stem cell-like lateral hypodermal (seam) cells.

143 ontracts and pulls together the edges of the hypodermal sheet at the ventral midline.

144 To investigate myotactin's role in muscle-hypodermal signaling, we characterized the myotactin loc

145 fusion protein was secreted from the apical hypodermal surface of the embryo.

146 podermal seam cells but not in the main body hypodermal syncytium (hyp7) that underlies, synthesizes,

147 ective in the anchoring of nuclei within the hypodermal syncytium and in the migrations of the two di

148 hat lin-35 activity is required in the major hypodermal syncytium and not in the VPCs to inhibit vulv

149 n between the vulval precursor cells and the hypodermal syncytium at an early larval stage.

150 NA expression over 200-fold in the main body hypodermal syncytium, hyp 7.

151 uires that the VPCs do not fuse to the major hypodermal syncytium, hyp7.

152 ongly in seam cells, rather than in the main hypodermal syncytium, indicating that seam cells play th

153 n "inhibitory signal" from the adjacent hyp7 hypodermal syncytium.

154 tion of the heterochronic gene lin-42 causes hypodermal terminal differentiation to occur precociousl

155 es known to be required for proper timing of hypodermal terminal differentiation.

156 that heme homeostasis in the extraintestinal hypodermal tissue was facilitated by the transmembrane p

157 ers showed that CeRh1 is mainly expressed in hypodermal tissue, although it is also in other cell typ

158 tion at defined locations in the surrounding hypodermal tissue, whereas DMA-1 acts as the cognate rec

159 substantial local swelling of the underlying hypodermal tissue.

160 BR2 is localized in epidermal and hypodermal tissues at the root apex.

161 lon-1 is expressed in hypodermal tissues, which is the focus of body size dete

162 for larval seam cell specification, and for hypodermal to seam cell fate transformations induced by

163 An examination of hypodermal, visceral, and circulatory muscle showed that