ライフサイエンスコーパス: ARS

1 ARS elements of Saccharomyces cerevisiae are the cis-act

2 ARS is genetically associated with mutations in the PITX

3 ARSs are ubiquitously expressed, essential enzymes respo

4 Corresponding proteins for the 17 ARS genes were identified in the platelet proteome, of w

5 gradients: phenylalanyl-RS (FRS), and the 9 ARSs that form the multi-ARS complex (MSC).

6 onary function test results before and after ARS revealed that of 5 patients, 4 (80%) had improvement

7 s after ARS; however, at 3 to 4 months after ARS, pH monitoring was still pathological in 18% of pati

8 S to 0.7% (P < 0.001) at 3 to 4 months after ARS; however, at 3 to 4 months after ARS, pH monitoring

9 implement routine long-term follow-up after ARS in pediatric patients with gastroesophageal reflux d

10 at 1 to 5 years, and at 10 to 15 years after ARS, 81%, 80%, and 73% of patients, respectively, were c

11 At 10 to 15 years after ARS, the number of patients with pathological reflux had

12 ts were symptom free at 10 to 15 years after ARS.

13 ss of the location of CARE enhancer, for all ARS genes there was constitutive association of RNA poly

14 being more efficient, only DS can act as an ARS in long-term assays.

15 deletion of DS, Raji ori could now act as an ARS in the long term.

16 ing sequences (ARSs) in eukaryotic cells, an ARS consensus sequence (ACS) has emerged for budding yea

17 lex class I and II molecules may generate an ARS-specific autoimmune response, which may be responsib

18 re transformed with DNA fragments lacking an ARS and homologous to only 50 bp of ADE2 added to the en

19 Deletion mapping of an ARS element linked to the HO gene of Saccharomyces cerev

20 ne-positive YAC clones were detected when an ARS element was incorporated into a vector, demonstratin

21 ch carried an additional C. glabrata CEN and ARS region for stable plasmid maintenance, did show regu

22 istal to the upper esophageal sphincter) and ARS.

23 features common to both DNA polymerases and ARSs are the use of multidomain architectures that segre

24 between the inflammatory myopathies and anti-ARS antibodies implies a role for the ARS molecules in t

25 Current artesunate (ARS) regimens for severe malaria are complex.

26 tion of transcripts encoding arylsulfatases (ARS), an extracellular polypeptide that may be important

27 t Raji ori, binds EBNA1; whereas both act as ARSs in short-term assays, with DS being more efficient,

28 More origins can initially act as ARSs than can be established.

29 cytoplasmic tRNA synthetases and associated ARS-interacting multifunctional protein genes.

30 Atypical ARS was defined as lack of symptoms or signs, a single s

31 h typical ARS in 202 (70%) and with atypical ARS in 88 (30%) patients.

32 Patients with atypical ARS were hospitalized 4 times more often compared with t

33 osed slightly earlier compared with atypical ARS, but this difference was not significant (P = .3).

34 me significantly decreased from 13.4% before ARS to 0.7% (P < 0.001) at 3 to 4 months after ARS; howe

35 whose samples had AR-V7-positive CTCs before ARS inhibition had resistant posttherapy PSA changes (PT

36 fic marker for response and outcomes between ARS inhibitors and taxanes.

37 l-tRNA synthetase (GluProRS), a bifunctional ARS of the MSC, has a regulated, noncanonical activity t

38 terial-yeast shuttle plasmid deleted of both ARS and CEN elements.

39 n of the solution pH and the pK(a)'s of both ARS and the arylboronic acid.

40 Phenylboronic acid (PBA) binds to both ARS and HbA1c via diol-boronic acid complexation.

41 , the rDNA ARS requires a match to the 11 bp ARS consensus sequence (ACS) and a broad non-conserved r

42 The essential 11-bp ARS consensus sequence (ACS) that binds the origin recog

43 xecution points was accompanied by small but ARS-dependent changes in DNA topology.

44 and increased CRF mRNA expression induced by ARS were restored by icv-injection of OXT.

45 DNA replication origins, specified by ARS elements in Saccharomyces cerevisiae, play an essent

46 conserved sequences in the S. carlsbergensis ARS elements revealed that the homologous sequences are

47 The S. carlsbergensis ARS elements were active both in S. cerevisiae and S. mo

48 enesis, it is unclear how mutant forms cause ARS dental anomalies.

49 egative human PITX2A K50E allele also caused ARS-like phenotypes.

50 Both yeast single-copy CEN/ARS and high-copy 2micro shuttle plasmids can be isolate

51 strongly with the activity of S. cerevisiae ARS elements, demonstrating the conservation of ARS acti

52 RS) that functions in a plasmid, but certain ARSs are silent as replication origins in their natural

53 nts; however, within chromosome III, certain ARSs near the transcriptionally silent HML locus show no

54 We have isolated and characterized ARS elements from a chromosome III recovered from an all

55 r comprehensively mapping and characterizing ARSs within a yeast genome.

56 Chordate ARSs have evolved distinctive features absent from ances

57 parent in the 228 phylogenetically conserved ARS elements among the six sensu stricto Saccharomyces s

58 that delete the E and I silencers containing ARS elements.

59 contribute to the neural circuit controlling ARS in the nematode Caenorhabditis elegans.

60 ics reveals that ten of the twenty cytosolic ARSs associate with ribosomes in sucrose gradients: phen

61 c activator also creates a SWI/SNF-dependent ARS.

62 a plausible explanation to the differential ARS activity observed in our previous mcm1-1 mutant expe

63 rent understanding of recessive and dominant ARS-mediated disease.

64 In contrast, dominant ARS-mediated diseases specifically affect the peripheral

65 In wild-type cells treated with HU, early ARS elements replicated but late ones did not.

66 We found that a suppressor element (ARS), previously identified in mouse AR and located in t

67 autonomously replicating sequence elements (ARS elements; potential replication origins) replicate d

68 Ablation of dopaminergic neurons eliminated ARS behavior, as did application of the dopamine recepto

69 signated ARS1 and ARS2) were found to encode ARS enzymes capable of accepting a variety of fatty acyl

70 Interestingly, mutations in genes encoding ARS enzymes have been implicated in a broad spectrum of

71 y several rice (Oryza sativa) genes encoding ARSs, which are likely involved in the production of def

72 eterozygosity for missense mutations in five ARS genes, which points to a shared mechanism of disease

73 We propose a mechanism for ARS in C. elegans in which dopamine, released in respons

74 ain-of-function mechanism is responsible for ARS-mediated neuropathy, or if a combination of these me

75 rep, was identified that can substitute for ARS, and multiple elements, termed mtc, could substitute

76 We identified one requirement for ARSs to be established: They must function efficiently e

77 replication origins varied widely, with four ARS elements active in < or = 10% of cells in the popula

78 Based on these data, KARS becomes the fourth ARS gene associated with CMT disease, indicating that th

79 Furthermore, ARS was affected by mutations in the glutamate receptor

80 Hematopoietic acute radiation syndrome (H-ARS) is characterized by severe myelosuppression, which

81 Like the efficient H4 ARS, the rDNA ARS requires a match to the 11 bp ARS cons

82 of the rDNA ARS was cold sensitive, like H4 ARS mutants that require additional energy to unwind the

83 ilar to the unwinding of mutations in the H4 ARS that stabilize the double helix in the DUE region an

84 rDNA ARS is not as easily unwound as the H4 ARS.

85 but unlike the easily unwound, wild-type H4 ARS.

86 Insertion of a single, heterologous ARS (ARS305) in place of the HML ARS cluster reconstitut

87 es individuals at low (ARS < or =1) or high (ARS > or =4) likelihood of complete resolution of hypert

88 In chromosome III, the HML ARS cluster (ARS302-ARS303-ARS320) and ARS301 flank the

89 These results suggest that, for the HML ARS cluster (ARS303, ARS320, and ARS302), inactivity of

90 ered replication fork pause sites at the HML ARS cluster and ARS301 by analyzing DNA replication inte

91 he elimination of the pause sites at the HML ARS cluster and at the copy of ARS305 inserted in place

92 e but activated the silent origin at the HML ARS cluster in a minority of cells.

93 Deletion of the HML ARS cluster led to loss of the pause site.

94 eterologous ARS (ARS305) in place of the HML ARS cluster reconstituted the pause site, as did multipl

95 The replication fork pause at the HML ARS cluster was independent of cis- and trans-acting mut

96 on of replication origin function at the HML ARS cluster, as well as at ARS301, the E silencer.

97 Thus, replication origin silencing at HML ARSs is mediated by active replication origins residing

98 al at HML, providing additional time for HML ARSs to fire as origins.

99 large-scale mutation screen of the 37 human ARS genes in a cohort of 355 patients with a phenotype c

100 enamel hypoplasia-consistent with the human ARS phenotype.

101 Class II ARS possess a unique catalytic domain fold, possess acti

102 facial region, the classic sites affected in ARS.

103 anscriptional mechanism that is defective in ARS.

104 s where the animals predominantly engaged in ARS behaviour were identified in both study areas.

105 evelopment involving Dlx2 gene expression in ARS patients.

106 ayed GE and increased CRF mRNA expression in ARS were abolished by icv-injection of BMI.

107 rturbed by missense PITX2 mutations found in ARS patients.

108 derpinnings of the enamel defect observed in ARS patients who carry PITX2 mutations.

109 Bi-allelic mutations in ARSs typically cause severe, early-onset, recessive dise

110 Transfection of constructs that included ARS element into AD cells reduced the transactivating ac

111 We found that individual ARS elements replicate at characteristic times, some ear

112 It is suggested that central OXT inhibits ARS-induced CRF mRNA expression via GABA(A) receptors in

113 re excluded because they were not initiating ARS or taxane therapy; and 18 were excluded for processi

114 children to receive a total dose of 12 mg/kg ARS as either a control regimen of five i.m. injections

115 CHK2) checkpoint kinase, both early and late ARS elements were able to replicate.

116 f the genes encoding mitochondrial-localized ARSs were weakly induced.

117 one deacetylase inhibitors restored the lost ARS-binding complex.

118 A mutant designated ars73a exhibited low ARS activity and failed to show increases in ECP76, LHCB

119 RS accurately identifies individuals at low (ARS < or =1) or high (ARS > or =4) likelihood of complet

120 synthetic DNA sequences that retain maximal ARS function.

121 e readily applied to understand and modulate ARS function in diverse systems.

122 ; in absence of fever, presence of 2 or more ARS symptoms or signs.

123 RS (FRS), and the 9 ARSs that form the multi-ARS complex (MSC).

124 ADE2-adjacent sequences, including a nearby ARS, copied from chromosomal DNA.

125 d ARS303 and in the process discovered a new ARS, ARS320.

126 First, a battery of known and novel ARS inhibitors was tested against Plasmodium falciparum

127 lid GE was measured under non-stressed (NS), ARS and CHS conditions.

128 earch (ARS) during foraging, but only 42% of ARS were associated with fishing vessels, indicating muc

129 data provide the first complete analysis of ARS elements and DNA replication origins on an entire eu

130 bryologic techniques to study the biology of ARS in a zebrafish model that uses transgenes to mark ne

131 and recapitulates ocular characteristics of ARS, including corneal and iris stroma maldevelopment.

132 elements, demonstrating the conservation of ARS activity and replication origin function in these tw

133 The deletion of ARS resulted in an eightfold increase in AR-promoter act

134 l phage M13 vector which allows detection of ARS (autonomously replicating sequence) function in clon

135 scanning to define molecular determinants of ARS function with single-nucleotide resolution.

136 Little is known about the evolution of ARS elements.

137 his finding explains the frequent failure of ARS assays in mammalian cells.

138 The identification of ARS elements and analysis of their function as chromosom

139 To complete the systematic identification of ARS elements on S. cerevisiae chromosome III, overlappin

140 eplication origins and causes instability of ARS-containing plasmids.

141 scription and demonstrates the first link of ARS with defective PITX2 protein interactions.

142 binding in vitro correlated with the loss of ARS activity in vivo.

143 ons for defining the molecular mechanisms of ARS mutations toward designing therapies for affected pa

144 es zebrafish a potentially powerful model of ARS, amenable to in vivo experimentation and development

145 the enamel defect in a novel mouse model of ARS.

146 Studies on short-term outcome of ARS in pediatric patients with gastroesophageal reflux d

147 The outcomes of ARS included symptomatic improvement.

148 The proportion of ARS behaviours associated with fishing boats were higher

149 ssible mechanism for the previous reports of ARS in patients with balanced translocations involving t

150 Screening of ARS patients identified an approximately 7600-kb deletio

151 d for the recovery and semiquantification of ARS in a stained monolayer by acetic acid extraction and

152 s flanking the minimal functional domains of ARSs.

153 To further explore the role of ARSs in CMT disease, we performed a large-scale mutation

154 cm1-1 mutant can be overcome for a subset of ARSs by the inclusion of flanking sequences.

155 Replication origins (ARSs) at internal Y' elements were found to fire in earl

156 actors that assemble at replication origins (ARSs).

157 This region shows sequence homology to other ARS elements.

158 RS and the MSC, and to a lesser extent other ARSs, localize to translating ribosomes, most strikingly

159 ith superior survival on taxane therapy over ARS-directed therapy in a clinical practice setting.

160 Parenteral ARS is associated with a risk of delayed anemia in Afric

161 e-dose i.m. and a three-dose i.v. parenteral ARS regimen with the standard five-dose regimen using a

162 men with mCRPC, 191 were evaluable (128 pre-ARS inhibitor and 63 pretaxane).

163 A second telomere-proximal ARS, from an X element, does not act as an origin in a w

164 al ACS element and DNA unwinding in the rDNA ARS are naturally impaired, suggesting that inefficient

165 unwinding, we found that the DNA of the rDNA ARS is not as easily unwound as the H4 ARS.

166 Unwinding of the rDNA ARS required additional energy, similar to the unwinding

167 Like the efficient H4 ARS, the rDNA ARS requires a match to the 11 bp ARS consensus sequence

168 Here we examined components of the rDNA ARS that might contribute to inefficient extrachromosoma

169 ivo extrachromosomal replication of the rDNA ARS was cold sensitive, like H4 ARS mutants that require

170 examined the essential ACS match in the rDNA ARS, which is known to be imperfect at one position.

171 DNA unwinding inherent in the wild-type rDNA ARS contributes to inefficient replication function.

172 formation, and represses initiation at rDNA ARSs.

173 nRNP L binds to this ARS motif and regulates ARS-containing exons; however, hnRNP L does not function

174 tors, blocked induction of the AA-responsive ARS genes.

175 an aminoacyl-tRNA synthetase-like ribozyme (ARS ribozyme), which was evolved in vitro.

176 Alizarin red s (ARS) is used as a redox indicator.

177 Alizarin red S (ARS) staining has been used for decades to evaluate calc

178 -containing, fluorescent dye Alizarin Red S (ARS) was probed.

179 lting 4-item aldosteronoma resolution score (ARS), 3 likelihood levels for complete resolution were i

180 ntify transiting and area-restricted search (ARS) behaviours, believed to indicate foraging activitie

181 viduals exhibited an Area-Restricted Search (ARS) during foraging, but only 42% of ARS were associate

182 Area-restricted search (ARS) is a foraging strategy used by many animals to loca

183 e local sampling and area-restricted search (ARS) rely on flexible movements.

184 t confers autonomously replicating sequence (ARS) activity on plasmids, which specifically initiate r

185 on of the autonomously replicating sequence (ARS) and centromere (CEN) elements that are normally bot

186 reliable autonomously replicating sequence (ARS) assay for isolating potential replicators, the iden

187 The yeast autonomously replicating sequence (ARS) assay has been a valuable tool in dissecting replic

188 erevisiae autonomously replicating sequence (ARS) consensus, raising the question of how they are rec

189 s of each autonomously replicating sequence (ARS) element.

190 ished for autonomously replicating sequence (ARS) elements in yeast in which the ARS consensus sequen

191 ncodes 11 autonomously replicating sequence (ARS) elements that function as chromosomal replicators.

192 tivity of autonomously replicating sequence (ARS) elements.

193 mosome as autonomously replicating sequence (ARS) elements; however, within chromosome III, certain A

194 (CEN) and autonomously-replicating sequence (ARS) regions.

195 ontain an autonomously replicating sequence (ARS) that functions in a plasmid, but certain ARSs are s

196 cation of autonomously replicating sequence (ARS)-containing plasmids in yeast cells.

197 romosomal autonomously replicating sequence (ARS)1 of Saccharomyces cerevisiae were detected at the n

198 The activation-responsive sequence (ARS) motif has previously been identified in several exo

199 o define autonomously replicating sequences (ARSs) in eukaryotic cells, an ARS consensus sequence (AC

200 o detect autonomously replicating sequences (ARSs) in human cells.

201 gle copy autonomously replicating sequences (ARSs) in plasmids.

202 variety of autonomous replication sequences (ARSs) in the presence and absence of SWI/SNF.

203 with the USDA Agricultural Research Service (ARS), is a comparative legume resource that integrates g

204 frames homologous to those that flank seven ARS elements of the S. cerevisiae chromosome.

205 The positions of seven ARS elements identified in this S. carlsbergensis chromo

206 plication intermediates of each of the seven ARS elements identified revealed that their efficiencies

207 A phenotypically less severe ARS mutant (without tooth anomalies), PITX2 R84W, has a

208 o administer an androgen receptor signaling (ARS) inhibitor or a taxane.

209 enes named the "aspirin response signature" (ARS) was associated with PFS in HV1 (r = -0.31, p = 0.03

210 contained proteins that produced a specific, ARS-binding complex, while this complex appeared to have

211 ying (GE) induced by acute restraint stress (ARS) for 90 min is completely restored following 5 conse

212 drome component of acute radiation syndrome (ARS) results from depletion of immature parenchymal stem

213 Typical acute retroviral syndrome (ARS) was defined as fever plus at least 1 symptom or sig

214 on associated with Axenfeld-Rieger syndrome (ARS) demonstrates reduced phosphorylation.

215 Axenfeld-Rieger syndrome (ARS) patients with PITX2 point mutations exhibit a wide

216 Patients with Axenfeld-Rieger Syndrome (ARS) present various dental abnormalities, including hyp

217 X2 associated with Axenfeld-Rieger syndrome (ARS) provided the first link of this homeodomain transcr

218 re associated with Axenfeld-Rieger syndrome (ARS), which involves ocular, dental, and umbilical abnor

219 re associated with Axenfeld-Rieger syndrome (ARS).

220 nt of one or more alkylresorcinol synthases (ARSs), type III polyketide synthases (PKSs) that produce

221 Here, we examine tRNA-aminoacyl synthetase (ARS) localization in protein synthesis.

222 ubunit of a multi-aminoacyl-tRNA synthetase (ARS) complex, has also been reported to stabilize p53 vi

223 potential of the aminoacyl-tRNA synthetase (ARS) family as a source of antimalarial drug targets.

224 ion of the entire aminoacyl-tRNA synthetase (ARS) gene family revealed that 16/20 of the genes encodi

225 ations in several aminoacyl-tRNA synthetase (ARS) genes have been implicated in inherited CMT disease

226 omponents are the aminoacyl tRNA synthetase (ARS) molecules.

227 Aminoacyl tRNA synthetases (ARS) catalyze the ligation of amino acids to cognate tRN

228 Aminoacyl-tRNA synthetases (ARSs) are responsible for charging amino acids to cognat

229 Aminoacyl-tRNA synthetases (ARSs) catalyze the attachment of specific amino acids to

230 e genes encoding aminoacyl-tRNA synthetases (ARSs) have been implicated in CMT disease primarily asso

231 Aminoacyl-tRNA synthetases (ARSs) join amino acids to their cognate tRNAs to initiat

232 In translation aminoacyl-tRNA synthetases (ARSs) recognize the identities of tRNAs and charge them

233 polymerases and aminoacyl-tRNA synthetases (ARSs) represent large enzyme families with critical role

234 The PITX2 T68P ARS mutant protein physically interacts with FoxJ1; howe

235 The PITX2 T68P ARS mutation occurs at a protein kinase C phosphorylatio

236 cupancy of Mcm1 in the C domain of telomeric ARSs is required for efficient initiation.

237 BV, functions in vivo but fails in long-term ARS assays.

238 It was shown that ARS preferentially reacted with the boronic (neutral, tr

239 Recent data suggest that ARS molecules and their proteolytic fragments generated

240 The ARS accurately identifies individuals at low (ARS < or =

241 The ARS DNA structural attributes evident in cells blocked a

242 The ARS was associated with death or MI in both patient coho

243 evidence that explores the links between the ARS molecules, inflammation, and apoptosis, with the aim

244 differ for different exons that contain the ARS core motif.

245 d anti-ARS antibodies implies a role for the ARS molecules in the pathogenesis of these syndromes.

246 oxidative stress, JTV1 dissociates from the ARS complex, translocates to the nucleus, associates wit

247 er either upstream of or downstream from the ARS consensus sequence (ACS).

248 r keratoderma, and recently mutations in the ARS (component) B gene have been identified in families

249 ngs support the notion that mutations in the ARS gene are pathogenic in mal de Meleda.

250 qter, and in a recent study mutations in the ARS gene have been identified in families with this diso

251 ch two different homozygous mutations in the ARS gene were identified.

252 have distinct coordination properties in the ARS ribozyme.

253 p </= 0.0002) was improved by including the ARS or 1 of its genes, ITGA2B.

254 monstrate that AA availability modulates the ARS gene family through modulation of transcription elon

255 Expression of the ARS dominant negative human PITX2A K50E allele also caus

256 Several of the ARS molecules and their proteolytic fragments generated

257 sis of the best characterized context of the ARS motif, namely the ESS1 sequence from CD45 exon 4, to

258 indicate a mechanism for the activity of the ARS mutant proteins in specific cell types and provides

259 Mutation of the ARS sequence or an adjacent Abf1p-binding site significa

260 Saccharomyces cerevisiae ORC recognizes the ARS (autonomously replicating sequence) consensus sequen

261 lly for B2 function showed similarity to the ARS consensus sequence (ACS).

262 ith maximal repression found adjacent to the ARS consensus sequence in the subtelomeric core X elemen

263 equence (ARS) elements in yeast in which the ARS consensus sequence [4] (ACS) constitutes part of the

264 onstrate that different mutations within the ARS motif affect specific aspects of regulatory function

265 lent mating-type locus HML, and all of these ARSs are silent as replication origins.

266 hnRNP L binds to this ARS motif and regulates ARS-containing exons; however, h

267 parate plasmids or as origins when all three ARS elements are present in a single plasmid is the same

268 r, then the relative activities of the three ARS elements as single origins within separate plasmids

269 ulation along a spectrum ranging from LDT to ARS.

270 The binding of PBA to ARS shifts its redox potential negatively.

271 hout detectable AR-V7-positive CTCs prior to ARS inhibition.

272 showed superior OS with taxanes relative to ARS inhibitors when AR-V7-positive CTCs were detected pr

273 ract to refluxate; these patients respond to ARS despite negative pH test results.

274 s of many amino acids provide a challenge to ARSs.

275 ith a ROS-inducer, such as arsenic trioxide (ARS), N-(4-hydroxyphenyl) retinamide (HPR) or dithiophen

276 or = 10% of cells in the population and two ARS elements active in > or = 90% of the population.

277 er, at their native locations, where the two ARSs are in a cluster with ARS302, the I silencer, no re

278 zed 4 times more often compared with typical ARS (43% vs 11%; P < .001).

279 PHI manifested with typical ARS in 202 (70%) and with atypical ARS in 88 (30%) patie

280 Patients with typical ARS were diagnosed slightly earlier compared with atypic

281 proximal exposure who subsequently underwent ARS, 13 patients (81%) had resolution of cough and 3 pat

282 Of 20 patients who subsequently underwent ARS, asthma symptoms improved in 18 (90%), and 6 of them

283 least 5 times a day, subsequently underwent ARS.

284 omparisons of the DNA sequences of unrelated ARS elements from different regions of the genome have r

285 versity analysis was carried out on the USDA-ARS C. baccatum germplasm collection using data from GIS

286 SoyBase, the USDA-ARS soybean genetic database, is a comprehensive reposit

287 the USDA/Agricultural Research Service (USDA/ARS), and the Eunice Kennedy Shriver National Institute

288 g a summary of a workshop hosted by the USDA/ARS Children's Nutrition Research Center and summary rep

289 llaborate in the repair of the genome, while ARSs provide aminoacylated tRNA precursors for protein s

290 re found to fire in early-mid-S phase, while ARSs at the terminal Y' elements were confirmed to fire

291 is for developmental defects associated with ARS patients.

292 are not considered typically associated with ARS, or occurrence of an opportunistic disease.

293 n typically considered to be associated with ARS; in absence of fever, presence of 2 or more ARS symp

294 However, when HbA1c competes with ARS for PBA binding, the solution potential shifts posit

295 However, the treatment of patients with ARS remains mostly supportive and palliative.

296 Here, we dissected two conserved telomeric X ARSs, ARS120 (XARS6L) and ARS131a (XARS7R), that replica

297 ation of a nearby replication origin, the Y' ARS.

298 An unfired Y' ARS, an inserted foreign (bacterial) sequence, and, as p

299 (HPV16) genome that can substitute for yeast ARS and CEN elements.

300 f these origins appears to require the yeast ARS consensus sequence and, as with yeast origins, addit