ライフサイエンスコーパス: epistasis

1 between a protein's amino acids ('intra-gene epistasis').

2 ire genetic background, a phenomenon called 'epistasis'.

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

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

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

6 ational strategies for learning the relevant epistasis.

7 n have a rich combinatorial structure due to epistasis.

8 creases the likelihood of identifying causal epistasis.

9 f beneficial fitness effects and patterns of epistasis.

10 ore broadly, they show strong pleiotropy and epistasis.

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

12 outperforms methods that do not account for epistasis.

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

14 to account for the strength of selection and epistasis.

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

16 pecificity for discovery of asthma genes and epistasis.

17 ation of rank orders that imply higher order epistasis.

18 ferentiation at loci involved in cytonuclear epistasis.

19 act the phenotypes of mutant strains through epistasis.

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

21 x, exhibiting both allelic heterogeneity and epistasis.

22 s without requiring a biased distribution of epistasis.

23 ditional mutations, which indicated negative epistasis.

24 interactions are evidence for true molecular epistasis.

25 vironment, which reveals rampant patterns of epistasis.

26 c context through gene interactions known as epistasis.

27 and adjacent nucleotides in SD show stronger epistasis.

28 moderate effects with significant polygenic epistasis.

29 on coefficient and the magnitude and type of epistasis.

30 y-used methods on detecting the ground-truth epistasis.

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

32 ational robustness, sequence degeneracy, and epistasis.

33 s restricting tolerated substitutions due to epistasis.

34 ss landscape and a preponderance of negative epistasis.

35 ture the effects of genomic interactions and epistasis.

36 en mutations within a full gene showing sign epistasis.

37 melanoma development is a result of negative epistasis.

38 s effect sizes, heritability, dominance, and epistasis.

39 ess landscape and a predominance of positive epistasis.

40 h of the single mutants, indicating negative epistasis.

41 ential approach to rank orders based on sign epistasis.

42 ng specific epistasis instead of nonspecific epistasis.

43 lioration of antagonistic pleiotropy through epistasis(13,14,20-22).

44 Negative epistasis (52%) occurred 7.6 times as frequently as posi

45 occurred 7.6 times as frequently as positive epistasis (6.8%).

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

47 work provides a systematic identification of epistasis affecting antibiotic resistance in N. gonorrho

48 However, even though epistasis affects the accessibility of maximum phenotypi

49 n the effect size of collateral sensitivity, epistasis among adaptive mutations, and fitness costs.

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

51 In the last example, higher order epistasis among four SVs affecting three related transcr

52 ations are necessary for further expansions, epistasis among host range mutations can potentially aff

53 rands, and a high frequency of negative sign epistasis among individually beneficial mutations.

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

55 Genetic epistasis among these factors revealed that Nfil3 expres

56 Epistasis analyses found that SaeRS and SrrAB influence

57 rexpression, structure-function, and genetic epistasis analyses indicate that these dendrite morphoge

58 Epistasis analyses indicated that moesin functions downs

59 Epistasis analyses reveal that FAN1 has cross-link repai

60 Epistasis analyses were conducted, and significant stati

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

62 y stages of the viral lifecycle, and genetic epistasis analysis demonstrated that the three genes fun

63 Epistasis analysis demonstrated that these contrasting r

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

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

66 Epistasis analysis has shown that AdrA acts upstream of

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

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

69 Epistasis analysis indicated that CDKA1 and Rb/E2F/Dp1 r

70 Epistasis analysis is an effective method to map genetic

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

72 Epistasis analysis places RAM1 downstream of CCaMK, CYCL

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

74 Epistasis analysis revealed that the Dsc E3 ligase acts

75 Epistasis analysis showed significant epistatic interact

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

77 Epistasis analysis suggests that PCNA over-accumulation

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

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

80 by similarity in phenomic profiles and used epistasis analysis to discover parallel networks centere

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

82 Epistasis analysis uncovered a uniquely interconnected g

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

84 ues and computational techniques to scale up epistasis analysis using Empirical Bayesian Elastic Net

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

86 One is that epistasis analysis will induce over-fitting of an over-s

87 comes from the intensive computing time for epistasis analysis, even when the appropriate model and

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

89 e-filter to narrow down the search space for epistasis analysis.

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

91 y additive epistasis, dominance by dominance epistasis and additive by dominance epistasis, and accou

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

93 uncovers the mechanistic basis for RET-EDNRB epistasis and emphasizes how functionally different gene

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

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

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

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

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

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

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

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

102 Patterns of epistasis and shapes of fitness landscapes are of wide i

103 Finally, we found evidence that both epistasis and the depletion of the pool of beneficial mu

104 ds the importance of gene-gene interactions (epistasis) and main effects of genes.

105 ominance epistasis and additive by dominance epistasis, and account for intrasubject fluctuations due

106 etic effects of dominance, dominance-related epistasis, and gene-ethnicity interactions on human body

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

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

109 zing genetic effects of additive, dominance, epistasis, and their ethnicity-specific effects.

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

111 ion loci are zero, incomplete penetrance and epistasis are a better explanation for the apparent 'rec

112 nd find that order perturbations beyond sign epistasis are prevalent in the antimalarial drug-resista

113 low-ups to detect interactions between SNPs, epistasis are still yet to be modeled and discovered mor

114 Genetic interactions such as epistasis are widespread in nature and can shape evoluti

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

116 s GenEpi, a computational package to uncover epistasis associated with phenotypes by the proposed mac

117 ed that GenEpi has the ability to detect the epistasis associated with phenotypes effectively and eff

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

119 hich are revealing the mechanistic causes of epistasis at different levels of biological organization

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

121 Whereas epistasis between adaptive substitutions has been studie

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

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

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

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

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

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

128 Here we report that positive epistasis between the coding and noncoding regions of th

129 er 68% of plumage variation was explained by epistasis between the gene NDP and a ~2.8-megabase regio

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

131 ibiotic class and measure experimentally the epistasis between tolerance and resistance mutations.

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

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

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

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

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

137 among mutations) because a high incidence of epistasis can reduce the accessibility of evolutionary p

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

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

140 We develop two new expression-epistasis centrality methods that incorporate interactio

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

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

143 We circumvented epistasis constraints among them using a combinatorial l

144 many microbial systems, diminishing-returns epistasis contributes to a tendency for more-fit genotyp

145 We find epistasis contributes to phenotypic variance widely.

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

147 tic background and that this idiosyncrasy in epistasis creates all of the above trends without requir

148 This "chain-breaking" epistasis creates sinkholes in SD fitness landscapes and

149 Therefore, the problem of identifying epistasis demands efficient statistical methods.

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

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

152 es, imputation strategies, meta-analysis and epistasis detection.

153 able and low-population proteins and, due to epistasis, direct the evolutionary pathways in an organi

154 n simultaneously handle additive by additive epistasis, dominance by dominance epistasis and additive

155 Epistasis emerges when the effects of an amino acid depe

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

157 crease with the time since its origin due to epistasis ("entrenchment"), but to decrease due to rando

158 We found widespread negative epistasis, especially in beta-strands, and a high freque

159 Using a variety of genetic tools and epistasis experiments in P. putida, we uncovered an 'ups

160 Epistasis experiments indicate a requirement for Spatzle

161 Epistasis experiments reveal that it functions upstream

162 Chemical genetic and epistasis experiments showed that GPER1 mediates the eff

163 Behavioral epistasis experiments suggest that aSP2 neurons may cons

164 y potential Rbpms2 targets and apply genetic epistasis experiments to decipher the genetic hierarchy

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

166 PP-InsP levels affect the ESR, we performed epistasis experiments with mutations in rpd3 and msn2/4

167 Epistasis experiments with Tdg-deficient mESCs show no i

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

169 Epistasis experiments, structure-function analysis, and

170 Here, using genomic approaches and epistasis experiments, we define the Sox17-governed endo

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

172 into co-expression, we recently developed an epistasis-expression network centrality method that blen

173 Epistasis for aggressive behavior causes cryptic genetic

174 s the emergence of pairwise and higher-order epistasis for fitness at loci underlying colour.

175 Here, we show that epistasis for fitness is an emergent and predictable pro

176 single amino acid substitutions to calculate epistasis for over 8000 mutation pairs.

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

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

179 strategies that illuminate how quantitative epistasis from modified gene dosage defines background d

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

181 polymorphisms under co-selective pressure or epistasis has received considerable recent attention in

182 landscape, but a clear picture of intragenic epistasis has yet to emerge.

183 n which resistance mutations interact, i.e., epistasis, has been extensively studied.

184 Our limited understanding of such epistasis hinders the correct prediction of the function

185 The statistical epistasis identified between CACNG5 and CACNG6 suggests

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

187 mental strategies to profoundly characterize epistasis in a protein, relevant to both natural and lab

188 nowledge, this is the first documentation of epistasis in a quantitative trait in Atlantic salmon.

189 Our results demonstrate the importance of epistasis in constraining adaptive paths.

190 Advancing our understanding of epistasis in crops can reveal new principles and approac

191 ting technologies are elevating the study of epistasis in crops.

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

193 We expect our general framework for the epistasis in killing conditions to be relevant for other

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

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

196 rther demonstrate the prevalence of positive epistasis in resistant genotypes, highlighting the impor

197 pairs of residues with the largest positive epistasis in the experiments are sufficient to determine

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

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

200 the ability of tree-based methods to detect epistasis in the presence of a polygenic signal.

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

202 Thus, the causes of epistasis in the wild remain poorly understood.

203 This deviation is due to epistasis, in which interactions between alleles are oft

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

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

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

207 d that our study would be surveying specific epistasis instead of nonspecific epistasis.

208 However, we show that, taking sign epistasis into account, leaps could become an important

209 About half of the discovered epistasis involved at least one locus previously associa

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

211 nian model to provide direct confirmation of epistasis involving many simultaneous mutations.

212 Epistasis is an important genetic foundation underlying

213 domestication and breeding, we highlight how epistasis is central in guiding the behavior of the gene

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

215 Epistasis is defined as a statistical interaction betwee

216 Epistasis is important in predicting phenotype from geno

217 Genetic epistasis is important in regulating biological function

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

219 n accessible for most phenotypes, even where epistasis is pervasive.

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

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

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

223 dout and constructed a viral host-dependency epistasis map (vE-MAP) of 356 human genes linked to HIV

224 Researchers should view current epistasis maps with caution until we better understand t

225 Polygenicity and epistasis may hinder efforts to identify genes and mecha

226 We present a subfunctionalization epistasis model to estimate the degree of functional red

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

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

229 exhibited a couple of hotspots for positive epistasis, most notably L221/ R222 at which many combina

230 method extends Katz centrality to expression-epistasis networks (EpistasisKatz), extends the Katz bia

231 ness landscapes that include reciprocal sign epistasis, no evolutionary dynamics-even ones that do no

232 We focus our analysis on the incidence of epistasis (non-additive interactions among mutations) be

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

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

235 Epistasis occurs due to nonlinearity in biological syste

236 These phenotypes are consistent with the epistasis of exo70A1 in the exo70A1 syp121 double mutant

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

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

239 ven among landscapes with no reciprocal sign epistasis; on these semismooth fitness landscapes, stron

240 se association with an outcome may be due to epistasis or statistical interactions with other feature

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

242 lemented, high-throughput methods to capture epistasis particularly at distal sites.

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

244 The term epistasis refers to interactions between multiple geneti

245 Epistasis reflects the distortion on a particular trait

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

247 Epistasis results from disruption of the continuous base

248 Finally, we show how the observed epistasis shapes the solution space of single-mutation t

249 ing the previous study of detecting marginal epistasis signals, and motivated by the universal approx

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

251 Chemical and genetic epistasis studies identified bone morphogenetic protein

252 Epistasis studies indicated that Rab11 is positioned dow

253 Indeed, epistasis studies place adipocyte-expressed Lrp4 and scl

254 Epistasis studies with C. elegans daf-2 mutants showed t

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

256 tions could be explained by identified loci, epistasis substantially increased explained phenotypic v

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

260 Patterns of epistasis that are shaped by ecologically based selectio

261 itive genetic basis but with some effects of epistasis that enhance differentiation between colour mo

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

263 Buried residues experienced more negative epistasis that surface-exposed residues.

264 site residues in the initial genotypes cause epistasis, that could lead to distinct evolutionary outc

265 However, GWAS techniques for detecting epistasis, the interactions between genetic variants ass

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

267 Understanding the pattern of epistasis-the non-independence of mutations-is critical

268 In addition, can epistasis-the source of landscape ruggedness and path co

269 The idiosyncratic epistasis theory explains the universalities in mutation

270 i identifies both within-gene and cross-gene epistasis through a two-stage modeling workflow.

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

272 the first to systematically examine pairwise epistasis throughout an entire protein performing its na

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

274 The contribution of epistasis to human disease remains unclear.

275 cate effects on LR, and both showed dominant epistasis to loci H and L, whereas H was epistatic to L.

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

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

278 ethods, C5.0 and logic regression, to detect epistasis under several simulated conditions, varying st

279 luorescent protein-an opportunity to examine epistasis up to the 13(th) order.

280 there are two major barriers in identifying epistasis using large genomic datasets.

281 In contrast, fitness epistasis was dampened in another treatment, where selec

282 al the prevalence and patterns of intragenic epistasis, we present a survey of epistatic interactions

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

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

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

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

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

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

289 onal, signed and weighted network of QTL-QTL epistasis, whose emergent properties reflect the ecologi

290 fficient and effective GWAS method to detect epistasis will be a key for discovering sophisticated pa

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

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

293 ae2-5A synergizes with mre11-nd and exhibits epistasis with sgs1Delta.

294 heir cognate templates, to uncover prevalent epistasis within the binding pocket of a human G protein

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.