ライフサイエンスコーパス: vasa

1 ding modes and affinities for both Par-4 and VASA.

2 Saccharomycescerevisiae Ded1p and Drosophila Vasa.

3 egulating other multipotency factors such as vasa.

4 indle-class gene similar to the RNA helicase Vasa.

5 spermatogonia or spermatocytes and expressed VASA.

6 ated a human ortholog of the Drosophila gene vasa.

7 hat express integrin-alpha-6 (IA6), pou3 and vasa.

8 the germ cell markers nanos3, dnd, dazl and vasa.

9 n silencing, and perinuclear localization of Vasa.

10 e similarity to the protein-coding host gene vasa.

11 In many species examined, Vasa, a DEAD-box RNA helicase, is found in these morphol

12 In addition, both KGB-1 and CSN-5 bind Vasa, a Drosophila germ granule component; therefore, si

13 Genes encoding two zinc finger proteins, Vasa, a LIM domain protein, Sox and Jun-like transcripti

14 Although GLHs are homologous to Drosophila VASA, a polar granule component necessary for oogenesis

15 AMPPNP structure, and that of the Drosophila Vasa*AMPPNP*Mg2+*RNA complex, we targeted 20 positions i

16 are large (> 10 mum) and stain positive for Vasa, an early germ line-specific protein.

17 er is nucleated by the DEAD box RNA helicase Vasa and contains the two Piwi proteins participating in

18 the regulatory sequence of medaka germ gene vasa and generated transgenic fish with visible GFP expr

19 By examining the expression of Strigamia vasa and nanos orthologues, we find that the primordial

20 ke two other known polar granule components, Vasa and Oskar, Aubergine remains cytoplasmic after pole

21 Using RNA interference we show that vasa and piwi are not required maternally or zygotically

22 lts add to the growing body of evidence that vasa and piwi can play important roles in somatic develo

23 us PGCs and absence of instructive roles for vasa and piwi in PGC formation are reminiscent of mouse

24 amine germ line development and the roles of vasa and piwi orthologues in the common house spider Par

25 These include vasa and piwi, which can play essential roles in any or

26 ess the germ-cell markers dazl, dnd, nanos3, vasa and piwil1 and the spermatogonial markers plzf and

27 script and protein expression patterns of Pt-vasa and Pt-piwi to show that primordial germ cells (PGC

28 e-related genes PRDM1, PRDM14, LIN28A, DAZL, VASA and SYCP3 induced direct conversion of somatic cell

29 ster transcripts immunoprecipitate with both Vasa and UAP56.

30 In Drosophila and Xenopus, Vasa and XVLP, respectively, are required for the establ

31 RNA pathway in regulating the levels of OSK, VASA, and possibly other genes involved in germline dete

32 In this study, we characterized vasa as a putative marker of germline precursors.

33 m cell-specific conditional knock-out (Cul4b(Vasa)),as well asCul4bglobal knock-out (Cul4b(Sox2)) mou

34 s developed normally and did not overexpress Vasa, as did embryos from a micromere deletion, implying

35 Vasa associates with the spindle and the separating sist

36 t association between WAGO-1 and a conserved Vasa ATPase-related protein RDE-12.

37 f mature germ cells, including expression of VASA, BOL, SCP1, SCP3, GDF9 and TEKT1.

38 and second-order originated from first-order vasa circumferentially around the vessel wall.

39 Here we show that the Vasa coding region is sufficient for its selective enric

40 We attempted to use the germline-expressed Vasa-Cre transgene to engineer a mouse mutation, but obs

41 w tool for genetic analysis of the germline, Vasa-Cre(ERT2), showed that this pathway functions throu

42 The Vasa DEAD-box helicases are widespread markers of germ c

43 The maternal RNAs vasa, dead end, nanos1, and daz-like all become localize

44 Furthermore, vasa deferentia from t-PA-null mice were hyporesponsive

45 MC proliferation in the central tail artery, vasa deferentia, seminal vesicles, prostate, and uterus,

46 tention of MD tissue in the epididymides and vasa deferentia.

47 Maelstrom protein is localized to nuage in a Vasa-dependent manner.

48 Interestingly, Maelstrom, but not Vasa, depends on two genes involved in RNAi phenomena, a

49 USTAVUS binding to the DEAD-box RNA helicase VASA (DINNNN).

50 stem cell population of the embryo, and that vasa expression in this embryo is restricted early by tr

51 on transplantation into fertile adults, thus vasa expression is correlated with the potential for gam

52 pleting maternal PIWI does not affect OSK or VASA expression or abdominal patterning but leads to fai

53 vasa expression was dynamic during asexual development i

54 In adults, vasa expression was observed in the gonads, as well as i

55 We show that ATP-dependent RNP remodeling by Vasa facilitates transfer of 5' sliced piRNA precursors

56 ms analyzed, Caenorhabditis elegans has four Vasa family members, the germline helicases GLH-1, GLH-2

57 In contrast, vasa from PAI-1-null mice were much more responsive (P<0

58 We therefore propose that UAP56 and Vasa function in a piRNA-processing compartment that spa

59 These results suggest that, when present, Vasa functions are essential to contributing to developm

60 In contrast to the single Vasa gene in most systems analyzed, Caenorhabditis elega

61 d adult tissues that expression of the human VASA gene is restricted to the ovary and testis and is u

62 sa gene, we find evidence for at least three vasa gene loci.

63 The vasa gene locus was duplicated from the original site an

64 a plasmid concentrations corresponded to the vasa gene, an important component of the nuage-piwi RNA

65 that Nile tilapia have a single copy of the vasa gene, we find evidence for at least three vasa gene

66 ed the zebrafish homologue of the Drosophila vasa gene, which, in the fly, encodes a germ-cell-specif

67 foundation for studying the role of multiple vasa genes in the development of tilapia gonads, and wil

68 stodes and trematodes have lost the piwi and vasa genes that are hallmark characters of the germline

69 nd sequencing of BAC clones for Nile tilapia vasa genes.

70 31, is expressed on GSCs and differentiating vasa(+) germ cells.

71 We discuss the evolution of the Vasa/GLH genes and current views of their functions and

72 Recent research suggests, however, that Vasa has a much broader function, including a significan

73 ing and export, whereas the DEAD box protein Vasa has an established role in piRNA production and loc

74 This absence of Piwi-like Agos and Vasa helicases prompts the question: how does the germli

75 The ATPase activity of Mouse Vasa Homolog (MVH) is essential for processing the inter

76 Furthermore, we find that the mouse Vasa homolog associates with Tudor domain-containing pro

77 Here, we report that mouse (mouse Vasa homolog), Xenopus laevis, and D. melanogaster Vasa

78 We have focussed on mouse vasa homologue (Mvh), a gene that is essential for male

79 Northern blotting revealed that zebrafish vasa homologue (vas) transcript is present in embryos ju

80 roduce abundant piRNAs that are antisense to vasa; however, vasa mRNA escapes silencing due to imperf

81 is necessary for the proper localization of Vasa, implying that Vasa is involved in the cyclin-depen

82 a previously hypothesized conserved role for vasa in cell cycle progression.

83 We identified that Vasa in the sea urchin is essential for: (1) general mRN

84 Here we identify vasa in two sea urchin species and analyze the regulatio

85 5 is required for the production of sDMAs of Vasa in vivo.

86 nt of the germ plasm associated protein DDX4/VASA in Xenopus embyos.

87 num homolog (Cf-vas) of the germ cell marker Vasa indicated that the B(4) blastomere in four cell-sta

88 We also learned that Vasa interacted with mRNAs in the perinuclear area and a

89 ll micromeres, whereas overexpression of the Vasa-interacting domain of Gustavus (GusDeltaSOCS) resul

90 , an ortholog of the Drosophila melanogaster Vasa intronic gene (VIG), is required for this process.

91 l retardation protein (FMRP), dFXR, and VIG (Vasa intronic gene), through their association with RISC

92 Vasa is a broadly conserved ATP-dependent RNA helicase t

93 Vasa is a broadly conserved DEAD-box RNA helicase associ

94 Vasa is a conserved RNA-helicase found in the germ lines

95 Vasa is a DEAD-box RNA helicase that functions in transl

96 vasa is a highly conserved RNA helicase involved in anim

97 Vasa is a key germ cell determinant in many animal speci

98 Curiously, Vasa is also present in the somatic cells of many animal

99 The RNA helicase Vasa is another essential protein in germline developmen

100 germ cell genome is activated, we find that vasa is expressed specifically in germ cells.

101 e proper localization of Vasa, implying that Vasa is involved in the cyclin-dependent cell cycle netw

102 the cyclin-dependent cell cycle network, and Vasa is required for the efficient translation of cyclin

103 Results herein indicate that Vasa is utilized widely, and often induced transiently,

104 uced Gurken accumulation and modification of Vasa - is very similar to the phenotype of the spindle-c

105 Transient vasa knockdown did not have obvious effects on germline

106 ing the maternal piwi dose increases OSK and VASA levels correspondingly and doubles and triples the

107 d Xenopus laevis; one example is the Xenopus Vasa-like protein (XVLP) [4-6].

108 ariant Rhino, that nuage granules containing Vasa localize directly across the nuclear envelope from

109 to target a reporter construct to the DDX4 (vasa) locus in chicken primordial germ cells (PGCs).

110 cells determined in early development, that vasa may function in an early stem cell population of th

111 in a profound heterochrony, suggesting that vasa might play a homeostatic role in asexual developmen

112 elstrom as a spindle-class gene that affects Vasa modification.

113 piRNAs that are antisense to vasa; however, vasa mRNA escapes silencing due to imperfect complementa

114 We found that maternally deposited vasa mRNA segregates early in development to a posterior

115 In contrast to vasa mRNA, which is present uniformly throughout all cel

116 umulate Vasa protein even though they retain vasa mRNA.

117 mulates in only a subset of cells containing vasa mRNA.

118 An overlapping set of genes, including vasa, nanos and piwi, operate in both multipotent precur

119 includes the classic germline lineage genes vasa, nanos and piwi.

120 c neuropathy results from destruction of the vasa nervorum and can be reversed by administration of a

121 n nerve function and limited the recovery of vasa nervorum and nerve function.

122 ts from microvascular ischemia involving the vasa nervorum and suggest the feasibility of a novel tre

123 graftment of EPCs in nerves and particularly vasa nervorum and their paracrine effects.

124 re was a profound reduction in the number of vasa nervorum associated with marked endothelial cell ap

125 ere uniquely localized in close proximity to vasa nervorum, and a smaller portion of these EPCs were

126 these drugs, resulting in destruction of the vasa nervorum, and accordingly that the neuropathy could

127 urbations affect neurons, Schwann cells, and vasa nervorum, which are held to be the primary cell typ

128 acrophages) and the endothelial cells of the vasa nervorum.

129 Neither Pt-vasa nor Pt-piwi gene products are localized asymmetrica

130 pectedly, we discovered AT-chX piRNAs target vasa of Drosophila mauritiana in the testes of interspec

131 ombination with the germ cell-specific mRNA, VASA (OSKMV).

132 B1 and SPSB4 bind strongly to both Par-4 and VASA peptides.

133 Knocking down Piwi1, Vasa, Pl10 or Ncol1 expressed by blastema cells inhibite

134 We show that a vasa/PL10 homolog is required for proliferation and main

135 ility to test the function of these putative VASA positive germ cells is limited, these results demon

136 mum); the A gate produced significantly more Vasa-positive cells (45.0% +/- 15.2%) than the "B" gate

137 Whereas Vasa presence is often indicated as a metric for germlin

138 A knockdown of Gustavus protein reduces both Vasa protein abundance and its propensity for accumulati

139 We find that vasa protein accumulates in only a subset of cells conta

140 ly throughout all cells of the early embryo, vasa protein accumulates selectively in the 16-cell stag

141 nes in isolated culture, including selective Vasa protein accumulation and transcriptional activation

142 has a conserved, positive regulatory role in Vasa protein accumulation during embryonic development.

143 egative cadherin each suggest that, although vasa protein accumulation in the small micromeres is fix

144 domain of Gustavus (GusDeltaSOCS) results in Vasa protein accumulation throughout the embryo.

145 Further, these cells do not accumulate Vasa protein even though they retain vasa mRNA.

146 , paraffin-embedded tissue and characterized VASA protein expression in human germ cells at various s

147 rated polyclonal antibodies that bind to the VASA protein in formalin-fixed, paraffin-embedded tissue

148 stricted to a few special cases, such as the Vasa protein in the fruit fly Drosophila.

149 inds the N-terminal and DEAD-box portions of Vasa protein independently.

150 The VASA protein is cytoplasmic and expressed in migratory p

151 he sea urchin Strongylocentrotus purpuratus, Vasa protein is enriched in the small micromeres despite

152 We found that Vasa protein is present in all blastomeres of the early

153 VASA protein is present in fetal and adult gonadal germ

154 Inhibition of Vasa protein synthesis interferes with proper chromosome

155 In this paper, I use immunodetection of Vasa protein to study germ cell development in the amphi

156 oved respond by significant up-regulation of vasa protein translation, followed by spatial restrictio

157 served germ plasm components, nanos mRNA and Vasa protein, revealed that germ plasm segregation is a

158 heir failure to retain Seawi transcripts and Vasa protein.

159 omolog), Xenopus laevis, and D. melanogaster Vasa proteins contain both symmetrical and asymmetrical

160 hese cells express germ cell markers such as vasa, pumilio and piwi, as well as sphingosine-1-phospha

161 movement through the walls of the ascending vasa recta (AVR) in the exposed papillae of 2-week-old S

162 ave suggested that the fenestrated ascending vasa recta (AVRs) drain the interstitial fluid in this l

163 ltage-operated Na+ conductance in descending vasa recta (DVR) pericytes isolated from the renal outer

164 nsport across the outer medullary descending vasa recta (OMDVR).

165 Histologic fibrosis of the medullary vasa recta and cortical interstitium was seen, but glome

166 eases [Ca2+]i in pericytes of the descending vasa recta as part of its constrictor action and that th

167 ferentiating outer medullary tubules and the vasa recta bundle area.

168 Disruption of the endothelium of the vasa recta by perfusion with latex microspheres enabled

169 nd descending limb of Henle epithelia and in vasa recta endothelia.

170 in were both expressed on the endothelium of vasa recta in the renal medulla, the lymph node subcapsu

171 nd low urea reflection coefficient of UT3 in vasa recta may be important for the formation of a conce

172 disease who showed peritubular capillary and vasa recta thrombi and capillary basement membrane alter

173 ([NO]i) of pericytes and endothelium of the vasa recta were independently measured with the use of f

174 ase of [NO]i of 19+/-6 U in pericytes of the vasa recta when the vessels were adjacent to medullary t

175 In isolated vasa recta with intact endothelium, Ang II reduced [Ca2+

176 Pericytes of isolated vasa recta without surrounding mTALs showed a rapid peak

177 elium of glomeruli, peritubular capillaries, vasa recta, and the principal cells (epithelial) of coll

178 urea rapidly as they traverse the ascending vasa recta, thereby preventing loss of urea from the med

179 nt exchange between ascending and descending vasa recta, to enhance the cortico-papillary osmolality

180 helial damage in peritubular capillaries and vasa recta.

181 the vascular bundles of the outer medullary vasa recta.

182 -sensitive NO production in pericytes of the vasa recta.

183 porter in erythrocytes and kidney-descending vasa recta.

184 titium, and medulla including vessels in the vasa recta.

185 the outer medulla is expressed in descending vasa recta.

186 l tubule, thin descending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the collecting duct;

187 nd mesangial cells, and tubules around adult vasa rectae express Ang-2.

188 as roles in maturation of both glomeruli and vasa rectae.

189 In the male germline, these vasa-related AT-chX repeats produce abundant piRNAs that

190 NPC)-like FG repeat domains are found in the VASA-related P-granule proteins GLH-1, GLH-2, and GLH-4

191 We show that pgl-1 and the glh (Vasa-related) gene family, which encode protein componen

192 Here, we report a mitotic function of Vasa revealed in the sea urchin embryo.

193 ponents, which include dead end, nanos1, and vasa RNAs, are initially present in a wide cortical band

194 These components assemble on the surface of Vasa's helicase domain, which functions as an RNA clamp

195 A VASA segment of Par-4 mediated its binding and degradati

196 Conversely, PAF, which contains this VASA segment, competitively bound to Fbxo45 and rescued

197 late of the mesenchyme blastula stage and Sp-vasa, Sp-nanos2, Sp-seawi, and Sp-SoxE transcripts are l

198 Also, in these injured arteries, the vasa spatial distribution was disrupted compared with no

199 Furthermore,Cul4b(Vasa)spermatozoa exhibited defective arrangement of axon

200 suggest an evolutionarily conserved role of Vasa that is independent of its function in germ line de

201 micromeres despite a uniform distribution of vasa transcript.

202 licase encoded by the "posterior" group gene vasa (vas) in control of localization of the mRNA encode

203 , we find that Bru interacts physically with Vasa (Vas), an RNA helicase that is a positive regulator

204 hetic axons embedded in a few arterioles and vasa vasora were recently shown to store tissue plasmino

205 espectively, P < 0.01) and in the density of vasa vasorum (1.84+/-0.05/mm2 vs. 4.73+/-0.24/mm2; respe

206 to neovascularization in the coronary artery vasa vasorum (VV).

207 ro-computed tomography techniques that image vasa vasorum anatomy in relation to the atheroma.

208 ed especially by an increase of second-order vasa vasorum and disorientation of normal vasa vasorum s

209 ansplanted islets received blood supply from vasa vasorum and had access to drainage through venous t

210 We observed more extensive vasa vasorum and intimal neovascularization in knockout

211 cytes and T lymphocytes, and the role of the vasa vasorum and surrounding perivascular adipose tissue

212 IP NCs arose directly from adventitial vasa vasorum and were anatomically and quantitatively re

213 The cellular origins of vasa vasorum are ill-defined and may involve circulating

214 nd with the development of vascular disease, vasa vasorum are known to develop.

215 Macrophages in the plaque and around vasa vasorum are reduced, but we detect no direct effect

216 onstrate that rPAI-1(23) treatment decreased vasa vasorum area and length, which was supported by mic

217 rPAI-1(23)-stimulated mechanisms that cause vasa vasorum collapse.

218 reconstructed confocal microscopy images of vasa vasorum demonstrate that rPAI-1(23) treatment decre

219 We observe vasa vasorum density correlates highly with the extent o

220 prevents the increase in VEGF expression and vasa vasorum density of coronary arteries in experimenta

221 Vasa vasorum density was higher in the HC group compared

222 lloon-injured coronary arteries, adventitial vasa vasorum density was increased (3.16+/-0.17/mm2 vs.

223 nned, and reconstructed, and quantitation of vasa vasorum density was performed.

224 Plaque size and vasa vasorum density were compared to 2 controls: mice f

225 a and disarray, and stenotic arteries in the vasa vasorum due to medial SMC proliferation.

226 are also vasculogenic and may be a source of vasa vasorum during atherogenesis.

227 ccount for the relative lack of intracranial vasa vasorum early in life.

228 culture adventitial fibroblasts (AdvFBs) and vasa vasorum endothelial cells (VVECs) from the adventit

229 ic cells and macrophages), progenitor cells, vasa vasorum endothelial cells and pericytes, and adrene

230 ctivity was found in luminal and adventitial vasa vasorum endothelium.

231 To inhibit growth of vasa vasorum in atherogenic mice and assess its effect o

232 Recent attention has focused on the role of vasa vasorum in atherosclerotic and restenotic coronary

233 The three-dimensional anatomy of the vasa vasorum in early coronary atherosclerosis is unknow

234 causes regression or collapse of adventitial vasa vasorum in hypercholesterolemic mice by stimulating

235 titate three-dimensional spatial patterns of vasa vasorum in normal and balloon injured porcine coron

236 ate the three-dimensional spatial pattern of vasa vasorum in normal and experimental hypercholesterol

237 ssessment of the therapeutic response of the vasa vasorum in patients with atherosclerotic plaque.

238 origin of plaque vasculature and the role of vasa vasorum in plaque growth.

239 We also studied the spatial growth of vasa vasorum in regions of neointimal formation.

240 Coronary arteries contain a network of vasa vasorum in the adventitia.

241 iew offers insight into the possible role of vasa vasorum in the development of intracranial vascular

242 These data demonstrate that formation of new vasa vasorum in vasculitis is regulated by inflammatory

243 arteries suggests that the formation of new vasa vasorum is determined by the nature of the immune r

244 ionally, neovascularization arising from the vasa vasorum may promote atherosclerotic plaque progress

245 es is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica m

246 mplex layer of the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune c

247 mplex layer of the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune c

248 pport a role for the endogenous ET system in vasa vasorum neovascularization in early coronary athero

249 in (ET) receptor antagonism reduces coronary vasa vasorum neovascularization in experimental hypercho

250 , a promoter of adventitial inflammation and vasa vasorum neovascularization in experimental models o

251 hanistic role of the endogenous ET system in vasa vasorum neovascularization in hypercholesterolemia

252 Cs, in a process involving ET-1, to regulate vasa vasorum neovascularization occurring in the adventi

253 ed phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaqu

254 molecular mechanisms regulating adventitial vasa vasorum neovascularization, which occurs in the pul

255 ede "macrovascular endothelial dysfunction." Vasa vasorum neovascularization, with endothelial leakag

256 increased, suggesting a mechanistic role for vasa vasorum neovascularization.

257 n the coronary arterial wall as well as with vasa vasorum neovascularization.

258 gests that adventitial neovascularization of vasa vasorum occurs in experimental hypercholesterolemic

259 Normal vasa vasorum originated from the coronary artery lumen,

260 growth factor-2 as mediators associated with vasa vasorum proliferation.

261 es of vasa vasorum were defined: first-order vasa vasorum ran longitudinally parallel to the vessel a

262 CML was localized to aortic and aortic vasa vasorum smooth muscle but not to collagen or elasti

263 er vasa vasorum and disorientation of normal vasa vasorum spatial pattern.

264 After 12 weeks, coronary vasa vasorum structure was assessed by three-dimensional

265 the quantitative response of the adventitial vasa vasorum to balloon-induced coronary injury.

266 -vessel vasculitis affecting branches of the vasa vasorum tree.

267 The density of newly formed vasa vasorum was proportional to vessel stenosis (r = 0.

268 ntiangiogenic effect of TSP-1, the number of vasa vasorum was reduced in aortas from diabetic rats.

269 Two different types of vasa vasorum were defined: first-order vasa vasorum ran

270 In normal arteries, vasa vasorum were restricted to the adventitia, but in i

271 to support development and maturation of the vasa vasorum within varying plaque types.

272 on," which is composed of dysfunction of the vasa vasorum's endothelium as well as "microcellular end

273 dventitia, particularly within microvessels (vasa vasorum) but not in cells of the intima or media.

274 al nitric oxide synthase (due to ingrowth of vasa vasorum), neointima formation, and loss of smooth m

275 ular adipose tissue promote expansion of the vasa vasorum, activation of fibroblasts, and differentia

276 f helping detect and even grade intracranial vasa vasorum, and this may provide new insights into our

277 hat the coronary vessel wall, especially the vasa vasorum, as well as bone marrow-derived endothelial

278 In conclusion, rPAI-1(23) inhibits growth of vasa vasorum, as well as vessels within the adjacent pla

279 from the artery lumen and outer adventitial vasa vasorum, deposit proatherogenic plasma molecules, r

280 ix can be imaged, as can angiogenesis of the vasa vasorum, plaque inflammation, and fibrin deposits o

281 Angiogenesis of the vasa vasorum, which are branches of bronchial arteries,

282 lammation; and to stimulate expansion of the vasa vasorum, which can act as a conduit for continued i

283 educed macrophage infiltration alongside neo vasa vasorum-like structure formation, reduced calcifica

284 atherogenic diet, suggestive of newly formed vasa vasorum.

285 use ECs line the vascular epithelium and the vasa vasorum.

286 from the development of immature neointimal vasa vasorum.

287 complete tissue integration and formation of vasa vasorum.

288 osclerotic plaque and associated adventitial vasa vasorum.

289 s the proliferation and intimal extension of vasa vasorum.

290 ural changes, including the formation of new vasa vasorum.

291 ssels, with proportionally more second-order vasa vasorum.

292 etween VEGF/VPF immunostaining and extent of vasa vasorum.

293 he ECM and altered formation of the coronary vasa vasorum.

294 Although the total number of vasa was increased after injury, the total vascular area

295 injury, the total vascular area comprised of vasa was significantly reduced in injured vessels compar

296 NA encoding the primordial germ-cell marker, vasa, was present for more than 30 days in embryo cells

297 sion of PGC markers nanos1 and TDRD7 but not vasa were down-regulated when dnd mutant proteins lackin

298 Two different types of vasa were found and classified as first-order or second-

299 he diameters of first-order and second-order vasa were smaller in normal compared with balloon-treate

300 SN5 mutations also cause the modification of Vasa, which is known to be required for Gurken translati