ライフサイエンスコーパス: autosome

1 on the X chromosome, whereas spe-5 is on an autosome.

2 ng its potential status as a non-recombining autosome.

3 A single linkage group spans each autosome.

4 provides single linkage groups spanning each autosome.

5 inkage if the X chromosome was treated as an autosome.

6 oci for coronary artery disease (CAD) on the autosome.

7 ale germline expression when relocated to an autosome.

8 Sex chromosomes originate from autosomes.

9 IM-5 protein localizes preferentially to the autosomes.

10 in crossover distribution on both the X and autosomes.

11 vement of genes from the X chromosome to the autosomes.

12 ted to the evolution of the X chromosome and autosomes.

13 the X chromosome, with lesser effects on the autosomes.

14 ysis of haplotype blocks across all 38 canid autosomes.

15 the Bogota X chromosome and one locus on the autosomes.

16 somes have many unusual features relative to autosomes.

17 d the enrichment of the male-biased genes on autosomes.

18 ecurrent duplication of retrogenes from X to autosomes.

19 fixation of male beneficial mutations on the autosomes.

20 y retroposition from the X chromosome to the autosomes.

21 mCH similar to the male X chromosome and the autosomes.

22 complex distinguishes the X chromosome from autosomes.

23 Sex chromosomes evolved from autosomes.

24 but instead were recruited secondarily from autosomes.

25 igher rate of evolution on the Y relative to autosomes.

26 n assigned to linkage groups on the cat's 18 autosomes.

27 ift than is expected from the pattern on the autosomes.

28 X chromosome and dominant-acting loci on the autosomes.

29 on both samples for 338 markers covering all autosomes.

30 omes replicating at a distinct time from the autosomes.

31 lved in eye development as that found on the autosomes.

32 elative to the ploidy, the number of sets of autosomes.

33 ence of its small size relative to the giant autosomes.

34 chromosome was more differentiated than the autosomes.

35 s variation among inbred strains than do the autosomes.

36 ent genomic loci located in X chromosome and autosomes.

37 art on genetic factors on both the X and the autosomes.

38 ications, ranking third in density among the autosomes.

39 riched across the X chromosome compared with autosomes.

40 on the sex chromosomes, but also on several autosomes.

41 ollectively mediate the behavior of the five autosomes.

42 tic interaction between the X Chromosome and autosomes.

43 y influenced by genetic variation present on autosomes.

44 enomic methylation patterns for all 22 human autosomes.

45 e silenced XY body, but also with unsynapsed autosomes.

46 ce of transcription factors on the X vs. the autosomes.

47 re balanced expression between the X and the autosomes.

48 o the weak positive correlation found on the autosomes.

49 nFeLV loci were detected across 12 of the 18 autosomes.

50 t and structure from each other and from the autosomes.

51 ely reported at the non-imprinted regions on autosomes.

52 .45% in 75-year olds), as reported for Y and autosomes.

53 ding comparison between the X Chromosome and autosomes.

54 panied the evolution of sex chromosomes from autosomes.

55 enes nor sufficient to repress transgenes on autosomes.

56 ee with experimental results for all GM12878 autosomes.

57 an ensemble of 3D structures for all GM12878 autosomes.

58 ers 100% female lethality when placed on the autosomes.

59 hree times lower on the X chromosome than on autosomes.

60 -specific spatial conformation distinct from autosomes.

61 X than seen for X-to-autosome retrogenes on autosomes.

62 e topology of X to a conformation resembling autosomes.

63 boundaries and more regular spacing than on autosomes.

64 d onto the X chromosome as compared with the autosomes.

65 ctor into permissive expression sites on all autosomes.

66 iversity-reducing selection on X than on the autosomes.

67 bers are largely consistent across all human autosomes.

68 the sex chromosome but also in trans of all autosomes.

69 ng their evolution from an ancestral pair of autosomes [1-4].

70 essive lethal in Jersey cattle on Bos taurus autosome 15.

71 When inserted on an autosome, a newly identified site can direct local MSL s

72 If the X chromosome is treated like an autosome, a sex difference in the phenotype can lead to

73 opied from sex chromosomes and inserted into autosomes, a process termed 'gene traffic'.

74 ng sex chromosome fuses to an autosome or an autosome acquires a new sex-determining locus/allele.

75 s that sex differences in DNA methylation of autosomes act as a primary driver of sex differences tha

76 ibed X chromosomes to one per diploid set of autosomes, allowing for dosage equality between the sexe

77 g, transcriptionally inactive regions on the autosomes also replicated in an unstructured manner, sim

78 ssed in somatic cells, Ant4 is encoded by an autosome and selectively expressed in testicular germ ce

79 use genome sequence, was 7.1-fold across the autosomes and 6.6-fold across the X chromosome.

80 ntly enriched on the X chromosome versus the autosomes and also occur at higher densities around X-li

81 erences in chromatin composition between the autosomes and between chromosome arms and centers.

82 n the X chromosome, creation of new genes on autosomes and changed genomic location of existing genes

83 Y chromosomes originate from ordinary autosomes and degenerate by accumulating deleterious mut

84 contents in comparison with both metatherian autosomes and eutherian chromosomes.

85 SET-domain protein MES-4 is concentrated on autosomes and excluded from the X chromosomes.

86 igh number of retrogenes that are located on autosomes and exhibit male-biased expression patterns [6

87 ago, Bridges proposed that male genes on the autosomes and female genes on the X chromosome compete t

88 s and compound heterozygous rare variants in autosomes and hemizygous rare variants in the X chromoso

89 veal that karyotype is a key factor: Smaller autosomes and heteromorphic sex chromosomes become weak

90 f coding sequence evolution on the X and the autosomes and illuminates interesting differences betwee

91 oth in the gene complements of the X and the autosomes and in the properties of the genes residing on

92 ted by their location on sex chromosomes vs. autosomes and inside vs. outside of Alu repeats, the for

93 Heterozygosity is restricted to autosomes and its retention is accompanied by substantia

94 enes located on the sex chromosomes than the autosomes and led to feminization of the X chromosome an

95 ecies boundaries as they diverge faster than autosomes and often have reduced diversity.

96 .3, 5q13-q22, and 11p15) have been mapped to autosomes and one gene (SOS1) has been associated with t

97 required in males for proper segregation of autosomes and provides a genetic tool for understanding

98 al problem of gene dosage imbalances between autosomes and sex chromosomes and also between males and

99 e coverage of 3.63- and 1.24-fold across the autosomes and sex chromosomes, respectively.

100 ce of single-nucleotide polymorphisms on the autosomes and sex chromosomes, will dramatically acceler

101 es' sex chromosomes are derived from ancient autosomes and show few signatures of their origins.

102 y in the chimpanzee X chromosome relative to autosomes and stronger purifying selection than for the

103 , Kind et al. show that MOF is also found on autosomes and that it has two modes of binding: one in m

104 sing a saturated linkage map spanning all 12 autosomes and the mitochondrion.

105 dual chromosomes and among chromosome types (autosomes and the two sex chromosomes).

106 Moreover, genes moving between the autosomes and the X chromosome experience change in seve

107 ective population size was estimated for all autosomes and the X chromosome from estimated LD between

108 Additionally, contrasting the autosomes and the X chromosome holds information on the

109 alyses 24 candidate genome regions within 14 autosomes and the X chromosome were revealed, in which 1

110 The resulting sex-averaged map covers 16 fox autosomes and the X chromosome with an average inter-mar

111 chanism for random monoallelic expression on autosomes and the X chromosome, and implicate Eed in est

112 g on regions of low marker density on feline autosomes and the X chromosome, in addition to regions f

113 with similarly prominent differences between autosomes and the X chromosome.

114 were analysed using 46,171 SNPs covering all autosomes and the X chromosome.

115 volved to counteract a similar effect on the autosomes and to prevent an overexpression of the X chro

116 of 40 independent intergenic regions on the autosomes and X chromosome comprising ~210 kb from each

117 e Y chromosome and the genetic background of autosomes and X chromosome.

118 te a persistent dosage imbalance between the autosomes and X chromosome.

119 Yet condensin I binds to autosomes and X chromosomes in both sexes to promote chr

120 hout the genome, with no strong bias between autosomes and X chromosomes.

121 ed the positions of TADs in human interphase autosomes and X chromosomes.

122 The Y chromosome evolved from an autosome, and its evolution has been characterized by ma

123 n of an ancestral sex-determining gene to an autosome, and the maintenance of multiple sex-determinin

124 loci (QTL) have been developed primarily for autosomes, and comparable methods for X-linked QTL have

125 ent with our reconstruction of the ancestral autosomes, and followed the evolutionary trajectory of a

126 k repair was delayed or failed in unsynapsed autosomes, and misexpression of chromosome X and chromos

127 genes, defined as those conserved on chicken autosomes, and newly acquired X-linked genes are upregul

128 y be different for the X chromosome than for autosomes, and so an X chromosome-specific significance

129 approximately 20-Mb intervals across the 19 autosomes, and three markers on the X chromosome.

130 rmed repeatedly across Diptera from ordinary autosomes, and X-chromosomes mostly conserve their ances

131 Genes on the autosomes are also implicated in blocking recombination.

132 nes remain suppressed postmeiotically, while autosomes are largely active.

133 r chromatids of X and Y chromosomes, but not autosomes, are segregated nonrandomly during asymmetric

134 one H3S10 kinase activity was able to rescue autosome as well as partially rescue male X polytene chr

135 ty and higher FST for Z-linked loci than for autosomes, as expected.

136 d nuclear elements (LINE)-1 (L1) along mouse autosomes at a 1-Mb scale, and found a unique combinatio

137 cusing on highly recombining portions of the autosomes, at a spatial scale appropriate to the study o

138 on to identify a gene affected by a balanced autosome;autosome translocation.

139 hromosomes may have originated from the same autosomes bearing the X allelic form that still exist in

140 an X and Y chromosomes evolved from ordinary autosomes beginning at least 180 million years ago.

141 s much more strongly differentiated than the autosomes between North American and African populations

142 le for Tef as a bridging molecule that holds autosome bivalents together via heterochromatic connecti

143 ysis identified a putative SNP on Bos taurus autosomes (BTA) 2 associated with phenotype 1, and anoth

144 completion, is less gene-dense than chicken autosomes but contains a massive tandem array containing

145 d, spermatogenesis genes are enriched on the autosomes but depleted on the X Chromosome (demasculiniz

146 Sex chromosomes originated from autosomes but have evolved a highly specialized chromati

147 The repeat is also present on autosomes but not on chromosome Y in other hominoid spec

148 (UBCS) are common near the telomeres of all autosomes but not the sex chromosomes.

149 fficient for correct chromosome targeting to autosomes but that both COOH- and NH(2)-terminal sequenc

150 Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensu

151 more pronounced on the X chromosome than the autosomes, but autosomal loci are also affected, possibl

152 X chromosomes evolve differently from autosomes, but general governing principles have not eme

153 osomes have evolved repeatedly from ordinary autosomes, but little is known about the processes that

154 chromosomes evolved from an ordinary pair of autosomes, but millions of years ago genetic decay ravag

155 Gene order is conserved on the autosomes, but noticeably less so on the Z chromosome, a

156 between the sexes, to a level equivalent to autosomes, by reducing Pol II recruitment to promoters o

157 though ectopic high-level Xist expression on autosomes can be compatible with viability, transgenic a

158 Comparisons of chromosome X and the autosomes can illuminate differences in the histories of

159 Autosomes carrying ectopic X-inactivation center sequenc

160 limb bones, we describe four QTLs located on autosome CFA 12, 30, 31, and X.

161 For pelvic shape we describe QTLs on autosome CFA 2, 3, 22, and 36.

162 l fluorescence in situ hybridization for the autosome chromosome 21 (chromosome 21 point probes combi

163 ; low divergence states cover inner parts of autosomes; chromosome X forms its own state with lowest

164 ther, these observations indicate that human autosomes contain discrete cis-acting loci that control

165 ion between an ancestral Z chromosome and an autosome corresponding to chromosome 15 in the Bombyx mo

166 higher than the rates of the paternal PAR or autosomes, culminating in an elevated chromosome-wide ra

167 The localization of HIM-5 to the autosomes depends on the activities of both xnd-1 and hi

168 tion in determining chromosomal locations of autosome-derived retroposed genes.

169 Available demographic models of X and autosome descent cannot account for the increased diverg

170 er reveal that the ratio of X chromosomes to autosomes dictates methylation levels, with female hybri

171 ome rearrangements involving eight different autosomes display delayed replication timing, and that c

172 We show that the difference between X and autosomes does not depend on the somatic dosage compensa

173 gene for lamin B1) have been shown to cause autosome-dominant leukodystrophy.

174 Here we showed that the autosome dose is communicated by a set of autosomal sign

175 chromosomes evolved from an ordinary pair of autosomes during the past 200-300 million years.

176 differences between the X chromosome and the autosomes either in the relative frequencies of mutation

177 animals (fem-3), a single pair of asynapsed autosomes elicits a checkpoint response, yet an unpaired

178 s diverged from mammals, different ancestral autosomes evolved into sex chromosomes in each lineage.

179 aptive evolution is barely detectable on the autosomes except for a few striking cases of recent sele

180 ial DNA rearrangements ensures that only one autosome expresses a functional T or B cell receptor.

181 chanism balances transcription between X and autosomes: expression of compensated hermaphrodite X-lin

182 mosome is evolving significantly faster than autosomes for nonsynonymous and most noncoding DNA sites

183 thereby marking somatic/progenitor genes on autosomes for repression.

184 structure and gene content of the ancestral autosome from which the sex chromosomes evolved.

185 These features were not present on the autosomes from which the Z and X chromosomes originated

186 The Z-autosome fusion brought two major genes conferring insec

187 is enhanced by rex site binding in cis in X-autosome fusion chromosomes.

188 [1]) and is very rapid after sex chromosome-autosome fusions in Drosophila [2-4].

189 retains only three percent of the ancestral autosomes' genes owing to genetic decay.

190 uggests that material from several different autosomes has been recently transferred to the sex chrom

191 diversity of the human X chromosome (X) and autosomes has facilitated understanding historical diffe

192 Y-linked gene loss through transposition to autosomes has previously been reported for a single isol

193 High density linkage maps for the porcine autosomes have been constructed exploiting the high dens

194 dures for Hardy-Weinberg equilibrium for the autosomes have been described, but Bayesian work on the

195 n MSL complex is ectopically localized to an autosome, histone H3K36 trimethylation (H3K36me3) is a s

196 e human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a

197 chromosomal arm 3L segregates as an ordinary autosome (i.e., two homologous copies in both males and

198 Integration of an Rsx transgene on an autosome in mouse embryonic stem cells leads to gene sil

199 that an ancient X chromosome reverted to an autosome in the lineage leading to Drosophila.

200 specifically-inherited X chromosome with the autosomes in 20 early Neolithic and 16 late Neolithic/Br

201 sity is about three-quarters of that for the autosomes in both species.

202 is stronger on the X chromosome than on the autosomes in chimpanzees.

203 may differ between the X chromosome and the autosomes in Drosophila melanogaster.

204 We find that fewer than half of the autosomes in each genome harbor all detectable introgres

205 ed duplicates generated from X chromosome to autosomes in flies and mammals.

206 e are higher on the X chromosome compared to autosomes in humans.

207 chromosomal copy number variations (CNVs) of autosomes in male subjects, whereas somatic loss of chro

208 eight cases of genes that have relocated to autosomes in mammalian lineages where the corresponding

209 ntified the frequency of aneuploidy of three autosomes in the cerebral cortex and cerebellum of adult

210 novel pathway that distinguishes the X from autosomes in the germ line, and further show that xnd-1

211 structure (F(ST)) were constructed from all autosomes in two large SNP data sets.

212 omes differentiated from different ancestral autosomes in various vertebrate lineages.

213 usual evolutionary stability of lepidopteran autosomes; in contrast, higher rates of intrachromosomal

214 -biased for all sex-linked genes relative to autosomes, including those in the pseudoautosomal region

215 Many X-autosome incompatibilities in natural populations may be

216 ther F1 male sterility is caused by X-Y or X-autosome incompatibilities or a combination of both.

217 e sterility appears to be caused mainly by X-autosome incompatibilities, X-Y incompatibilities contri

218 male-beneficial duplicates are biased toward autosomes, independent of the dominance parameters of se

219 -mediated regulation may contribute to the X-autosome interaction.

220 sults imply a significant role for Y/X and Y/autosome interactions in maintaining proper expression o

221 Ectopic X-autosome interactions inhibit endogenous X-X pairing and

222 In order to detect Y chromosome-autosome interactions, which may go unnoticed in a singl

223 t gene transposition from sex chromosomes to autosomes is a conserved phenomenon across mammalian spe

224 Random monoallelic expression on the mouse autosomes is broadly similar to that in human cells: it

225 e exception to the UBCS pattern found in all autosomes is chromosome 2, which shows a UBCS peak midch

226 The other set of autosomes is discarded into a residual body.

227 tic diversity on chromosome X to that on the autosomes is sensitive to both natural selection and dem

228 transgenes inserted into X chromosome versus autosome locations.

229 this approach was able to produce a targeted autosome loss in aneuploid mouse embryonic stem cells wi

230 single X, unlike asynapsed X chromosomes or autosomes, maintains repressive chromatin marks and rema

231 Sex chromosomes evolved from autosomes many times across the eukaryote phylogeny.

232 ting forces between the X chromosome and the autosomes may be associated with various pathologies cau

233 osatellite markers distributed across the 22 autosomes (mean intermarker distance, 9.2 centimorgans).

234 The bias of X-to-autosome movement was significantly stronger for RNA-bas

235 mentation, including the X-chromosome and an autosome (Muller Element C/E).

236 enes--EIF1AX/Y and RPS4X/Y--transposition to autosomes occurred independently in three distinct linea

237 ved papaya sex chromosomes with a homologous autosome of a close relative, the monoecious Vasconcelle

238 up and were probably inherited from a single autosome of an ancestor.

239 Here we show that an autosome of Drosophila, the dot chromosome, was ancestra

240 omosome of F. virginiana and the homeologous autosome of hermaphroditic diploid species.

241 ORI-29 library has an average depth over the autosomes of 5.0-fold and 2.8-fold coverage of the X chr

242 loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell

243 A1 deposition are largely similar across the autosomes of both cell lines.

244 Unexpectedly, DPY-21 also associates with autosomes of germ cells in a DCC-independent manner to e

245 ed genes is much lower than that of genes on autosomes: on average, maximal expression is three times

246 se if an existing sex chromosome fuses to an autosome or an autosome acquires a new sex-determining l

247 their autosomal insertion induces de novo X-autosome pairing.

248 significantly lower rate of recombination on autosomes, possibly due to the presence of polymorphic a

249 in a way that is different from that of the autosomes, potentially resulting in accelerated evolutio

250 rrent models invoke a dependency on the X-to-autosome ratio (X:A), but molecular factors remain poorl

251 selection can account for the observed X to autosome ratio of variability in the ancestral populatio

252 servations: notably, the puzzlingly low X-to-autosome ratios of substitution rates in humans and chim

253 errepresentation of male-biased genes on the autosomes recently observed in microarray expression exp

254 on of retrogenes on the X than seen for X-to-autosome retrogenes on autosomes.

255 as well as differences in sex chromosome vs. autosome segregation.

256 reas two subpopulations were observed in the autosomes separating gynodioecy and dioecy and three sub

257 ster chromatids, which co-segregate with the autosome set to generate a functional haplo-X sperm.

258 In all cases, insertions on the autosomes showed significantly higher expression than th

259 individual Y genes inserted as transgenes on autosomes shows that expression of the Zfy 1/2 paralogs

260 ore likely to produce male sterility than on autosome (so-called large-X theory); second, spermatogen

261 For autosomes, some 44% of these SNPs have a minor allele fr

262 essions show a significant enrichment on the autosomes, supporting an epistatic interaction between t

263 allele (Mybl1(repro9)) had subtle defects in autosome synapsis in pachynema, a high incidence of unsy

264 mutation-selection balance conditions for X-autosome synthetic lethals and steriles.

265 Second, we analyze sex chromosome versus autosome TE densities corrected for regional genomic eff

266 eterious mutations) is more effective on the autosomes than on the X chromosome, because of the lack

267 that there are more genes subject to RMAE on autosomes than the number of genes on the X chromosome w

268 o random monoallelic expression on mammalian autosomes than there are on the X chromosome and that th

269 nly 2% of the MSY derives from the ancestral autosomes that gave rise to the mammalian sex chromosome

270 tic interaction between the X Chromosome and autosomes that is essential for male fertility.

271 X or Z-linked divergence exceeds that on the autosomes (the so-called 'faster-X effect').

272 rphic sex chromosomes evolved from a pair of autosomes, the sex chromosomes became increasingly diffe

273 es X chromosome dose relative to the sets of autosomes, the X:A ratio.

274 by the ratio of X chromosomes to the sets of autosomes, the X:A signal.

275 es share features that distinguish them from autosomes: the acquisition and amplification of testis-e

276 Y chromosomes evolved from a single pair of autosomes, they are highly differentiated: the Y chromos

277 la miranda is in transition from an ordinary autosome to a genetically inert Y-chromosome, while its

278 Similarly, autosome-to-X retroposition events are associated with l

279 e Y-linked genes have autosomal paralogs, so autosome-to-Y transposition must be the main source of D

280 NA methylation profiling in six unbalanced X;autosome translocations.

281 TEX11-deficient spermatocytes with asynapsed autosomes undergo apoptosis at the pachytene stage, whil

282 eparately on the Bogota X chromosome and USA autosomes using a combination of different mapping strat

283 6 regulate the different chromatin states of autosomes versus X chromosomes and are required for germ

284 l, X and Y chromosomes evolve from a pair of autosomes via a series of inversions leading to stepwise

285 ith polymorphic markers across the 19 murine autosomes was performed on the N2 mice.

286 nd that monoallelic DNA accessibility across autosomes was pervasive, developmentally programmed and

287 e nuclear-nuclear (specifically X chromosome-autosome), we found the strongest deleterious interactio

288 unnoticed in a single-species background of autosomes, we constructed hybrid genotypes involving thr

289 nearly always involved in tangles, and small autosomes were involved more often than large ones.

290 somes have evolved from a pair of homologous autosomes which differentiated into sex determination sy

291 s undergo mosaic events more frequently than autosomes, which could have implications for understandi

292 es have unequal ratios of sex chromosomes to autosomes, which has resulted in the invention of divers

293 aches we detect 199 peaks spread over all 19 autosomes, which potentially contribute to trait variati

294 methods designed to investigate gene flow in autosome-wide genotype data from 3,528 unrelated individ

295 It is the largest human autosome with orthology to only a single mouse chromosom

296 d Ware culture show high similarity in their autosomes with European hunter-gatherers, Steppe Eneolit

297 ian ZW pair is believed to have evolved from autosomes, with most change occurring in the chromosomes

298 Also, for X chromosome-to-autosome (X-->A) movement, we observed high testis expre

299 s of development, and in strains harboring X;autosome (X;A) fusions.

300 nicate the ratio of X chromosomes to sets of autosomes (X:A signal).

301 All three are members of autosome/X gene pairs.