ライフサイエンスコーパス: epistasis

1 urther increase in primary root length (i.e. epistasis).

2 t genetic effects or gene-gene interactions (epistasis).

3 sets respond in different ways (called mixed epistasis).

4 hrough maps both with and without high-order epistasis.

5 interactions are evidence for true molecular epistasis.

6 vironment, which reveals rampant patterns of epistasis.

7 c context through gene interactions known as epistasis.

8 outperforms methods that do not account for epistasis.

9 moderate effects with significant polygenic epistasis.

10 on coefficient and the magnitude and type of epistasis.

11 lleles at other sites, a phenomenon known as epistasis.

12 x under purifying selection are enriched for epistasis.

13 mportance of stability effects in functional epistasis.

14 timates of h(2) due to shared environment or epistasis.

15 sms for occurrences of positive and negative epistasis.

16 uence space can be significantly expanded by epistasis.

17 n abscission ("skirt") phenotype, suggesting epistasis.

18 ress up a rugged fitness landscape involving epistasis.

19 ess the problem of mapping sterile loci with epistasis.

20 blicly available at: http://biomecis.uta.edu/epistasis.

21 ditive variance is consistent with pervasive epistasis.

22 s with little-to-no detectable pleiotropy or epistasis.

23 se positive in the identification of QTL and epistasis.

24 to account for the strength of selection and epistasis.

25 ts itself as subtle but pervasive high-order epistasis.

26 ation of rank orders that imply higher order epistasis.

27 ferentiation at loci involved in cytonuclear epistasis.

28 act the phenotypes of mutant strains through epistasis.

29 e-locus selective sweeps with linkage but no epistasis.

30 x, exhibiting both allelic heterogeneity and epistasis.

31 ditional mutations, which indicated negative epistasis.

32 unctionalization characterized by long-range epistasis, a promiscuous intermediate, and few gain-of-f

33 owing evidence for the pervasiveness of sign epistasis--a complete reversion of mutational effects, p

34 tematic comparison of mutational effects and epistasis across a wide range of bacterial species.

35 ontrast, on single-peak landscapes that lack epistasis, all uphill paths converge.

36 We find that the presence of epistasis allows natural selection to mould the distribu

37 etic and zygotic LDs indicate the absence of epistasis among CNV loci.

38 exists for synergistic as well as disruptive epistasis among loci.

39 ted in other species, few examples exist for epistasis among natural polymorphisms in human traits.

40 co-modulated target loci, in the absence of epistasis among them, which produces a cluster of linked

41 Genetic epistasis analyses demonstrate that SHREC subunits and t

42 Instead, epistasis analyses demonstrate that the tailless H2A/H3

43 Epistasis analyses found that SaeRS and SrrAB influence

44 Epistasis analyses indicated that moesin functions downs

45 Epistasis analyses reveal that FAN1 has cross-link repai

46 Genetic epistasis analyses suggest that Wise requires Lrp4 to ex

47 Epistasis analyses were conducted, and significant stati

48 pathway and their modes of regulation using epistasis analyses-a powerful tool that was quickly adop

49 , few methods are available for quantitative epistasis analysis and epistasis-based network reconstru

50 y factors involved in DNA repair, we perform epistasis analysis and show that REV3-mediated resistanc

51 in HR sub-pathways, we carried out extensive epistasis analysis between mutants defining Rrp1/2, Rad5

52 Epistasis analysis demonstrated that these contrasting r

53 Moreover, epistasis analysis demonstrates that PAXX functions toge

54 Combining GWAS and epistasis analysis driven by statistical and knowledge-b

55 Large-scale quantitative epistasis analysis has been well established for single

56 Genetic epistasis analysis in Hfx. volcanii suggests that NreA w

57 athway, we performed a comprehensive genetic epistasis analysis in the yeast Saccharomyces cerevisiae

58 Epistasis analysis indicates that ETR1 and EIN4 function

59 Epistasis analysis indicates that several of these loci

60 Epistasis analysis is an effective method to map genetic

61 Epistasis analysis is an essential tool of classical gen

62 ble, high-throughput method for quantitative epistasis analysis of developmental phenotypes.

63 Epistasis analysis places RAM1 downstream of CCaMK, CYCL

64 Gene expression and epistasis analysis reveal that the growth phenotypes of

65 Surprisingly, genetic epistasis analysis revealed that DTKR function was upstr

66 Epistasis analysis revealed that the Dsc E3 ligase acts

67 Furthermore, epistasis analysis revealed that while both contribute t

68 Epistasis analysis reveals that 9-1-1 complex components

69 Epistasis analysis showed significant epistatic interact

70 Genetic epistasis analysis showed that Reln(CTRdel)/Apoer2(null)

71 and Sec13) suppresses mTORC1 signaling, and epistasis analysis shows that GATOR2 negatively regulate

72 re hypersensitive to UV light, a defect that epistasis analysis suggests may result from less-effecti

73 In summary, through epistasis analysis this work uncovered an important role

74 e we present a method to extend quantitative epistasis analysis to developmental traits.

75 mented an expression quantitative trait loci epistasis analysis to explore the association between th

76 Here, we use genetic epistasis analysis to identify proteinase-activated rece

77 Epistasis analysis uncovered a uniquely interconnected g

78 lowed by a rigorous single and double-mutant epistasis analysis using CRISPR/Cas9-mediated engineerin

79 Toward this aim, epistasis analysis was carried out in which the phenotyp

80 Finally, via epistasis analysis, we demonstrate that PTEN and FANCD2

81 The approach is founded on epistasis analysis.

82 designed a novel synthetic biology 'in situ epistasis' analysis in which H3 dimethylated on lysine 4

83 y hairpins, we quantify widespread molecular epistasis and a long-hypothesized, structure-dependent p

84 on variance via two distinct modes of action-epistasis and destabilization.

85 ing a saturated mixed linear model including epistasis and environmental interaction, we identified a

86 loci that influence ear traits, with little epistasis and environmental interactions, totally accoun

87 relative fitness was primarily influenced by epistasis and epistasis x environment interactions.

88 expended into determining the importance of epistasis and epistatic variance for complex traits, the

89 Chemical-genetic epistasis and expression profiles revealed that both com

90 can be an intermediate step to discover both epistasis and gene by environment effects (GxE).

91 analysis, based on a linear mixed model with epistasis and gene-environment interaction effects, were

92 ts of natural selection change over time, as epistasis and historical contingency alter the strength

93 ovation via HGT is profoundly constrained by epistasis and historical contingency, similar to the evo

94 ffects are sufficient to predict the sign of epistasis and its environmental dependence.

95 interpreting the biological significance of epistasis and pleiotropy is often difficult.

96 n, protein structure, protein stability, and epistasis and quantitatively depicts the different costs

97 Together, epistasis and the genetic code create a pattern of conne

98 cent directions in methodology for detecting epistasis and to discuss evidence of the role of epistas

99 us factors, including multiple risk alleles, epistasis, and epigenetic effects such as methylation.

100 ex chromosomes, local adaptation, dominance, epistasis, and mate choice.

101 ntered upon the standard genetics concept of epistasis, and propose major questions that future studi

102 ny QTLs, large phenotypic effects, pervasive epistasis, and readily identified genetic variants.

103 nd derived genotypes, the prevalence of sign epistasis, and the number of local fitness maxima, are d

104 ent data from functional imaging, behavioral epistasis, and unilateral activation experiments that su

105 ression study design, that many instances of epistasis are found between common single nucleotide pol

106 is found in other organisms in which such an epistasis assay was performed, only few genes were highl

107 duce regeneration and to regulate TEP and JI Epistasis assays show that voltage-gated Na(+) channels

108 torial dimensionality reduction and Bayesian epistasis association mapping.

109 eveal the prevalence of metabolism-dependent epistasis at all regulatory levels.

110 able for quantitative epistasis analysis and epistasis-based network reconstruction.

111 ns revealed a pattern of diminishing-returns epistasis: Beneficial mutations have consistently smalle

112 Here we test the hypothesis that mixed epistasis between a gene pair can be explained by the ac

113 Whereas epistasis between adaptive substitutions has been studie

114 ddition, we identify intracohort synergistic epistasis between alleles of hsl7 and kel1, which arose

115 No strong evidence was found for any epistasis between antigens driving population dynamics,

116 obust conclusions from these studies is that epistasis between beneficial mutations often shows a pat

117 ions are shedding light on the statistics of epistasis between evolved mutations.

118 We describe the structural basis of sign epistasis between G238S and R164S, two adaptive mutation

119 of these individuals depends on intergenomic epistasis between larvae and nursing adults, explaining

120 d act additively, we also found evidence for epistasis between loci for clasper bristle number.

121 model offers the correct null prediction for epistasis between mutations across DNA-binding sites.

122 the importance of other factors such as the epistasis between mutations increasing the adaptation to

123 While epistasis between pairs of mutations is known to be an i

124 n by sequence substitution is constrained by epistasis between residues.

125 of functional variants in sequence space and epistasis between residues.

126 Our results support epistasis between SPINK5 and TSLP, which contributes to

127 and effects of sterile genes, as well as the epistasis between sterile genes.

128 ions - an effect arising from intermolecular epistasis between the transcription factor and its DNA-b

129 ;Grhl3(+/-)) murine embryos failed to detect epistasis between the two genes, suggesting that they fu

130 ntermediate phenotype, suggesting a role for epistasis between the underlying genes.

131 In this study, we reveal that the epistasis between Themis1 and Vav1 controls the occurren

132 mportance of the signaling pathway involving epistasis between Themis1 and Vav1 in the control of Tre

133 We found that while reciprocal sign epistasis blocked many direct paths of adaptation, such

134 Counter-intuitively, intermolecular epistasis can alleviate the constraints of individual co

135 These results illustrate that epistasis can be functionally multi-directional and non-

136 In large part, this epistasis can be qualitatively attributed to the structu

137 Our results suggest that intergenomic epistasis can be the proximate mechanism for social para

138 e that high-throughput mapping of intragenic epistasis can identify key structural and functional fea

139 Epistasis can profoundly influence the process of evolut

140 suggest that the environmental dependency of epistasis can profoundly influence the response to selec

141 genome scan to search for a pair of QTL with epistasis can suffer from low statistical power and also

142 text of Wright's adaptive landscape, genetic epistasis can yield a multipeaked or "rugged" topography

143 e of traits (such as linkage, dominance, and epistasis) can either drive or constrain speciation [1-3

144 This context dependence (epistasis) can reduce the probability of convergence and

145 s effects from two or more mutations, termed epistasis, can result in compensation of deleterious mut

146 Epistasis causes hidden quantitative genetic variation i

147 s-including the mean and SD of selection and epistasis coefficients-it was often unable to explain th

148 ce (10%), second (7%) and third (1.7%) order epistasis components.

149 In this analogy, epistasis constrains evolution, with some mutations tole

150 g and neutralizing similar cases of negative epistasis could improve productivity in many agricultura

151 We propose a new method, named cuckoo search epistasis (CSE) for identifying significant epistatic in

152 sed with cell-cycle progression, and genetic epistasis demonstrated that Ssp1 promotes mitotic entry

153 Here, we propose a new algorithm for fast epistasis detection based on hierarchical representation

154 implemented our method in a tool named EPIQ (EPIstasis detection for Quantitative GWAS), and we show

155 mpared other state-of-the-art tools for fast epistasis detection, LinDen drastically reduces the numb

156 ow to map quantitative trait loci (QTL) with epistasis efficiently and reliably has been a persistent

157 ve observations, this method of quantitative epistasis enabled detection of new interactions involvin

158 sed for heterosis: dominance, overdominance, epistasis, epigenetics, and protein metabolite changes.

159 Genetic epistasis experiments and analysis of tumor-derived miss

160 Epistasis experiments combining deletions of individual

161 Epistasis experiments further demonstrated that Wingless

162 Epistasis experiments indicate a requirement for Spatzle

163 Epistasis experiments indicate that Epk1 acts upstream o

164 mes and EGFR target genes are not expressed; epistasis experiments place the function of Vps4 at the

165 Epistasis experiments reveal that it functions upstream

166 Epistasis experiments show that silencing these transcri

167 Behavioral epistasis experiments suggest that aSP2 neurons may cons

168 Here, we use a series of epistasis experiments to show that Lm211 modulates neure

169 Phenotypic analyses, epistasis experiments, and in vitro phosphorylation assa

170 Based on epistasis experiments, SMG-1 does not appear to act in a

171 Epistasis experiments, structure-function analysis, and

172 Specifically, epistasis explains a quarter of the identified evQTLs, o

173 Epistasis for aggressive behavior causes cryptic genetic

174 onse of a diploid population is increased by epistasis, for a given initial genotypic variance.

175 ories, we computationally removed high-order epistasis from experimental genotype-fitness maps contai

176 ferent sublines, we demonstrated substantial epistasis from these naturally occurring variants.

177 tailless H2A/H3 phenotypes are in the RAD18 epistasis group, which regulates postreplication repair.

178 Quantitative genetic epistasis has been hypothesized to be an important facto

179 The statistical epistasis identified between CACNG5 and CACNG6 suggests

180 DNA binding, accurately predicts the sign of epistasis in a canonical cis-regulatory element consisti

181 tasis and to discuss evidence of the role of epistasis in human complex trait variation.

182 udy establishes the occurrence of biological epistasis in humans and provides mechanistic insight int

183 Recent evidence shows the importance of epistasis in individual evolutionary pathways.

184 iple deviations are caused by pleiotropy and epistasis in metabolism.

185 s and estimate a minimal effect of polygenic epistasis in modulating major risk alleles.

186 of millions of years predicted the extent of epistasis in our data, indicating congruence between the

187 present an efficient algorithm for detecting epistasis in quantitative GWAS, achieving a substantial

188 arily focused on duplicates essentiality and epistasis in several laboratory conditions.

189 hese mutations clearly illustrate a role for epistasis in shaping the emergence and subsequent evolut

190 -binding protein to explore the structure of epistasis in simulations of protein sequence evolution.

191 We also discuss the relevance of epistasis in the context of GWASs and potential hazards

192 etwork inferred from an analysis of pairwise epistasis in the DGRP.

193 The role of epistasis in the genetic architecture of quantitative tr

194 Despite a prevalent pattern of negative epistasis in the landscape, we find that the global fitn

195 istic combinations as we observed a positive epistasis in the majority of the combinations with samba

196 occur in lymphoma and leukemia despite their epistasis in the methylation-hydroxymethylation pathway.

197 ence diversity is made possible by pervasive epistasis in the RBS 220-loop and can be buffered by avi

198 ative contribution of the polygenic score vs epistasis in variation explained.

199 loped a new method to map sterile genes with epistasis in wide hybridizations of plants using a backc

200 tence of fitness holes and the prevalence of epistasis, including cases of sign and of reciprocal sig

201 d that the frequency of mutations exhibiting epistasis increases along the evolutionary pathway.

202 Furthermore, we showed that epistasis increases the variation explained above the co

203 individual mutation effects (and patterns of epistasis) influence paths taken at evolutionary "forks

204 The extent to which epistasis influences complex traits and contributes to t

205 description of pairwise/tertiary intragenic epistasis involving adaptive mutations.

206 ilding pairwise count tables for genome-wide epistasis is 1.0% more efficient.

207 Epistasis is a key factor in evolution since it determin

208 ven though this proportion can be high where epistasis is antagonistic to direct effects, it reduces

209 site evolves independently, indicating that epistasis is common in the evolution of gene regulation.

210 These studies indicate that epistasis is common, and that additivity can be an emerg

211 ose resulting from rpb9Delta alone, and this epistasis is consistent with the idea that defects cause

212 Epistasis is defined as a statistical interaction betwee

213 Epistasis is important in predicting phenotype from geno

214 Genetic epistasis is important in regulating biological function

215 Thus, the study of epistasis is of great interest to geneticists.

216 Epistasis is pervasive in viruses, affects the shape of

217 , we show that although significant positive epistasis is rare, many deleterious mutations are benefi

218 assuming no mutation or dominance, and that epistasis is symmetrical overall.

219 Epistasis is the interactions among multiple genetic var

220 Epistasis is the phenomenon whereby one polymorphism's e

221 ive interaction between genetic variants, or epistasis, is a possible explanation for the gap between

222 on lift works best under diminishing-returns epistasis, is not affected by problems of genetic load,

223 We further find that high-order epistasis makes it impossible to predict evolutionary tr

224 Hence multilocus epistasis makes substantial contributions to the additiv

225 Epistasis may be important in understanding the genetic

226 Then, we propose a novel generic epistasis model that provides a flexible solution for va

227 genotypes, for both single marker model and epistasis model.

228 ing methods for both single marker model and epistasis model.

229 pistasis, which is more common than positive epistasis, mostly occurs between combinations of destabi

230 The importance of epistasis--non-additive interactions between alleles--in

231 onally important, nonconserved positions; 5) epistasis (nonadditivity) among multiple mutations; and

232 oser analysis revealed that the magnitude of epistasis, not its order, predicts is effects on evoluti

233 ng the covariance between individuals due to epistasis of any order.

234 ns, revealing a dramatic context dependence (epistasis) of designed mutations in homologous protein-p

235 ions, epigenetic changes, somatic mutations, epistasis, oligogenic and polygenic hypotheses.

236 To determine the effect of high-order epistasis on evolutionary trajectories, we computational

237 leaf size and most resulted from a positive epistasis on growth.

238 At a single field site, the impact of epistasis on relative fitness varied significantly over

239 In this review we describe the effect of epistasis on the topology of evolutionary pathways that

240 roach is not susceptible to biases caused by epistasis or shared environment.

241 The importance of epistasis-or statistical interactions between genetic va

242 used increased Yki activity, and our genetic epistasis places dCsk downstream of Dachs.

243 We reveal that extensive epistasis prevents reversions and necessitates fixation

244 We therefore conclude that high-order epistasis profoundly shapes evolutionary trajectories th

245 The term epistasis refers to interactions between multiple geneti

246 the evolutionary consequences of high-order epistasis remain poorly understood.

247 retical possibilities, owing largely to sign epistasis requiring evolutionary steps that would entail

248 While epistasis reveals dependencies between genetic variants,

249 reviously reported a case of reciprocal sign epistasis (RSE), where two mutations individually increa

250 al selection and gene interactions (that is, epistasis) shape the evolution of mutational processes a

251 We found that high-order epistasis strongly shapes the accessibility and probabil

252 Epistasis studies using activated CED-10 and MIG-2 indic

253 SDS resistance, genome-wide association and epistasis studies were performed using a population of 2

254 their resident terminal selector and genetic epistasis studies with H3K9 methyltransferases suggest t

255 he functional dependence between genes in an epistasis study, which is an important role in inferring

256 We show that common measures of epistasis, such as the number of monotonically increasin

257 tubulin acetyltransferases; and (3) genetic epistasis suggests the microtubule-stabilizing protein T

258 itionally propose several best practices for epistasis testing to protect future studies from confoun

259 y when they should be quiescent, and genetic epistasis tests demonstrate that ectopic Cyclin E/Cdk2 a

260 Epistasis tests revealed that the dominant active SYMRK

261 mutants for the TGFbeta receptor baboon, and epistasis tests showed that baboon is epistatic to Smad2

262 Moreover, Yki activity reporters and epistasis tests showed that Yki does not mediate the key

263 ween the sensory neurons results in cellular epistasis that is reflected in their transcription of in

264 is not a realistic biological model and that epistasis (that is, the statistical interaction between

265 son's argument to show that, for any form of epistasis, the total response of a haploid population is

266 Epistasis-the non-additive interactions between differen

267 hrough conditional association analyses, and epistasis through interaction analyses.

268 cterize the extent and magnitude of pairwise epistasis throughout an entire protein molecule.

269 analysis of protein localization and genetic epistasis to dissect the structure of this network in Dr

270 The contribution of epistasis to human disease remains unclear.

271 mental designs to detect the contribution of epistasis to quantitative trait phenotypes in model orga

272 Our study highlights the utility of genetic epistasis to unravel the complexities of JAZ-TF interact

273 xtensively, relatively little is known about epistasis under purifying selection.

274 relative prevalence of the various kinds of epistasis varies along an adaptive walk.

275 Local genetic epistasis was detectable for a small proportion of CpG s

276 The SPINK5 and TSLP epistasis was replicated in a black population (P = .036

277 Using genetic epistasis we established here that Ihog and Boi, and the

278 (2) To test the hypotheses of epistasis, we adopt a new conditional permutation proced

279 cally survey a model landscape of intragenic epistasis, we quantified the fitness of ~60,000 Saccharo

280 selection response can only be increased by epistasis when some initially deleterious alleles become

281 many instances of both positive and negative epistasis when these interactions scaled to higher dimen

282 Epistasis (where the 'best' amino acid at one site depen

283 High-order epistasis-where the effect of a mutation is determined b

284 d undesirable branching and sterility due to epistasis, which breeders overcame with suppressors.

285 on pairs exhibited statistically significant epistasis, which had a strong negative bias, except when

286 ity analysis shows that significant negative epistasis, which is more common than positive epistasis,

287 In part, this might be due to epistasis, which is often not considered.

288 The narrowness is enhanced by epistasis, which was detected in up to 30% of genotypes

289 variant showed strong genetic and functional epistasis with allelic variants in IL7R exon 6.

290 flammatory disorder Behcet's disease (BD) in epistasis with HLA-B*51, which is the main risk factor f

291 ing selection are subsequently entrenched by epistasis with later substitutions: They become increasi

292 ve degeneracy in the PhoQ-PhoP interface and epistasis, with the effect of individual substitutions o

293 Our results show pervasive positive epistasis within a conformationally dynamic network of r

294 We found that rampant epistasis within and between the two molecules was essen

295 ed empirical evidence for the propensity for epistasis within VWF and showed strong correlation to co

296 Epistasis x environment interactions accounted for up to

297 eractions control fitness, the influences of epistasis x environment interactions on adaptive trait e

298 se genes to test the impact of epistatic and epistasis x environment interactions on adaptive trait v

299 varied significantly over 2 yr, showing that epistasis x environment interactions within a location c

300 ss was primarily influenced by epistasis and epistasis x environment interactions.