ライフサイエンスコーパス: epistatic

1 notypes every pairwise mutant interaction is epistatic.

2 Epistatic analyses demonstrate that Notch3 function lies

3 Epistatic analyses demonstrated that the expression of c

4 Moreover, epistatic analyses in vivo showed that dosage perturbati

5 gnaling is elevated in Pten cKO retinas, and epistatic analyses placed Pten downstream of TgfbetaRII

6 polymorphisms (SNPs), polygenic scores, and epistatic analyses.

7 Epistatic analysis demonstrated that Pck2 mediated, at l

8 Epistatic analysis indicates that DMAP1 acts in parallel

9 Epistatic analysis revealed a pathway in which Rho regul

10 Lastly, epistatic analysis revealed that PTP-3 is upstream of SY

11 Epistatic analysis, metabolic assays, and flux analysis

12 cluster expression is controlled via complex epistatic and allelic interactions between rDNA haplotyp

13 eratively modulated Top1cc turnover in a non-epistatic and ATM kinase-independent manner.

14 TM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nucl

15 atic GSL defense genes to test the impact of epistatic and epistasis x environment interactions on ad

16 Here we examine whether epistatic and gene-by-environment interactions have shap

17 ains a major hurdle given various associated epistatic and pleotropic effects.

18 complex traits are found to be regulated by epistatic and polygenic variants.

19 Nearly 80% of yield-associated QTL were epistatic, and contained between 0 and 44 annotated gene

20 ng of a combination of polygenetic, plastic, epistatic, and gene-environment interactive effects, as

21 d model algorithm for exhaustive genome-wide epistatic association analysis by controlling multiple p

22 a function of the ERAP1 context, explain the epistatic association of both molecules in ankylosing sp

23 We sought to determine independent and epistatic associations between filaggrin (FLG), serine p

24 ties and instead support an interchromosomal epistatic basis to hybrid female sterility.

25 m, the key enzyme(s) and its pleiotropic and epistatic behavior(s) responsible for low-molecular-weig

26 es, including Alzheimer's disease (AD), have epistatic causes, requiring more sophisticated analyses

27 ddition of specific pairwise- and high-order-epistatic coefficients decreased the predictive power of

28 disruptive mutational insults by cis-acting epistatic compensations.

29 with the polygenic score were tested for an epistatic component using a training set (n = 170), whic

30 to single markers, polygenic components and epistatic components.

31 We demonstrate, for the first time, epistatic constraint in an RNA virus due to host range m

32 nsidering a single final resistant genotype, epistatic contingencies among mutations restrict evoluti

33 Such a study is vital to identify epistatic couplings among residues that can provide usef

34 An epistatic effect between CYP11A1 and VDR polymorphisms m

35 es, we demonstrate that D95E mutation has an epistatic effect on the motifs involved in Stl binding.

36 for kinship matrix calculations and main and epistatic-effect genome scanning employ parallel computi

37 sets showed both concordance of direction of epistatic effects (P = 5.56 x 10(-31)) and enrichment of

38 Analyses that incorporate sex-dependent and epistatic effects could reconcile past inconsistencies a

39 However, estimating epistatic effects for quantitative traits is challenging

40 his study shows the necessity of considering epistatic effects in soybean SDS resistance breeding usi

41 loci may be considerably improved by taking epistatic effects into account.

42 l scan-revealing the individual and pairwise epistatic effects of every mutation to our model protein

43 , and we were able to identify both main and epistatic effects of genetic variants associated with tr

44 erval mapping and to examine independent and epistatic effects of Taar1 and Oprm1.

45 nly 0.3% was contributed by the marginal and epistatic effects of the SNPs in the intergenic area.

46 cated that TaVrt2 and TaVrn1 had significant epistatic effects on flowering time.

47 ly cooccurring alleles at these loci display epistatic effects on herbivore resistance and fitness in

48 C, FACT, and TFIIS, resulting in synergistic/epistatic effects on plant growth/development.

49 istance due to avirulent races, or they have epistatic effects on qualitative disease resistance gene

50 osomes of 1, 3, 6, 8 and 10, and significant epistatic effects were found among the four pairs of ste

51 modeling non-dosage dependent and intragenic epistatic effects when predicting expression.

52 enetic architecture (additive, dominant, and epistatic effects) of potential QTLs for growth traits i

53 ion of patients would empower the search for epistatic effects, and how network and cellular models m

54 nt analyses and genome scanning for main and epistatic effects.

55 ges in the magnitude and sign of fitness and epistatic effects.

56 tic effects (PEPIS), for analyzing polygenic epistatic effects.

57 gh breeding strategies based on additive and epistatic effects.

58 intly fitted all the additive, dominance and epistatic effects.

59 s geometric model is common in detecting the epistatic effects.

60 nd moderately overlap each other, suggesting epistatic effects.

61 and gun1 mutations evoke similar patterns of epistatic effects.

62 ric functional map, allowing pleiotropic and epistatic enzymatic explanation of PAH metabolism.

63 is review discusses the current evidence for epistatic events and genetic interactions in neuropsychi

64 termining a recessive or dominant link among epistatic expression quantitative trait locus to enable

65 sistently specifying signals as additive and epistatic for larger sizes.

66 ells, we demonstrate that TDP1 and PARP1 are epistatic for the repair of Top1cc.

67 ty of LMW PAH-centric hydroxylation, and its epistatic functional contribution is also crucial for th

68 is known to be governed by both dominant and epistatic gene action, its expression is greatly influen

69 focal adhesion and secretion is affected by epistatic gene copy number variation and it is predictiv

70 esence of recombinational suppressors and/or epistatic gene interactions in the MAT-CEN intervening r

71 quantitative tools to make inferences about epistatic gene interactions when the fitness landscape i

72 leneck frequently encountered in genome wide epistatic genetic effect analysis and enable accommodati

73 rver-based tool, the Pipeline for estimating EPIStatic genetic effects (PEPIS), for analyzing polygen

74 The epistatic genetic interactions observed among BEACH homo

75 ion was primarily influenced by additive and epistatic genetic variation, leaf damage was primarily i

76 gonorrhoeae and a generalizable approach for epistatic genome-wide association studies.

77 reduces the number of tests required for an epistatic genome-wide association study of antibiotic re

78 Genome-wide association (GWAS) and epistatic (GWES) studies along with expression studies i

79 The dominance and epistatic hierarchies of key loci governing this diversi

80 oth local ruggedness and amino acid-specific epistatic hotspots and that inference is additionally co

81 Moreover, Tim and DDX11 are epistatic in promoting efficient resumption of stalled D

82 t the NEIL3 and the FA/BRCA pathways are non-epistatic in psoralen-ICL repair.

83 We conclude that epistatic incompatibilities between human and archaic al

84 festation of these impacts can be subject to epistatic influences of the global genetic background.

85 The epistatic interaction analysis revealed significant inte

86 A forward genetics approach revealed how an epistatic interaction between a zeta-carotene isomerase

87 man genetic association analyses revealed an epistatic interaction between CYFIP1 and WAVE signaling

88 Epistatic interaction between FcGR polymorphisms and int

89 Our results show an epistatic interaction between IGHG1 and FCGR3A such that

90 The epistatic interaction between K33S and F427I thus may mi

91 cation and characterization of an intragenic epistatic interaction between the attenuating F427I muta

92 Further analysis revealed an epistatic interaction between the UL and US regions.

93 t enrichment on the autosomes, supporting an epistatic interaction between the X Chromosome and autos

94 additional insights into virulence gene and epistatic interaction discovery in HSV-1.

95 basis of hidden additive genetic effects and epistatic interaction effects, and we indicate opportuni

96 Further analysis detected an epistatic interaction for neovascularization between a s

97 ases, we pairwise deplete them generating an epistatic interaction map, evaluate cell cycle perturbat

98 This epistatic interaction of rare and common variants define

99 Together, our results uncover a novel epistatic interaction that regulates Dorsal dynamics by

100 We attribute this epistatic interaction to four other genes within the D.

101 l possible combinations; and (2) how to test epistatic interaction when all potential combinations ar

102 .09; 95% CI, .01-.73), suggesting a negative epistatic interaction which contrasts previous findings.

103 typing for the LRRTM4 region demonstrates an epistatic interaction with the CPQ region for ascites ph

104 e to alter phenotypic variation alone and in epistatic interaction with the nuclear genetic variation

105 well as a novel Parkinson's disease-specific epistatic interaction, all indicative of faster motor pr

106 Interestingly, Prr1 and Prr2 had a strong epistatic interaction, which also varied in the strength

107 nduced liver tumorigenesis, indicating their epistatic interaction.

108 g the functional and evolutionary effects of epistatic interactions across molecular interfaces.

109 In both scenarios, epistatic interactions affect the long-term response to

110 Epistatic interactions among genes can give rise to rugg

111 HERC2/OCA2 genes, respectively) and several epistatic interactions among independently associated al

112 Epistasis analysis showed significant epistatic interactions among Pto-miR257 and its targets.

113 In addition, processes including epistatic interactions and compensatory evolution, cosel

114 ecent studies that have probed the extent of epistatic interactions and have begun to chart the fitne

115 nificant main effect loci and 24 significant epistatic interactions associated with SSR resistance, w

116 ctions and, leveraging this ability, dissect epistatic interactions between cholesterol biogenesis an

117 However, several studies have now identified epistatic interactions between common variants that incr

118 requires interactions between loci, negative epistatic interactions between divergent regulatory elem

119 inor changes in signal levels lead to strong epistatic interactions between EGF and Notch.

120 Negative epistatic interactions between genes from different pare

121 we investigate whether there is evidence for epistatic interactions between genetic variants within t

122 e patterns have locked in early (such as the epistatic interactions between groESL and a constellatio

123 These epistatic interactions between homeoalleles are analogou

124 Analysis of epistatic interactions between jazQ and phyB reveal that

125 sky-Muller (BDM) incompatibilities involving epistatic interactions between loci contributed to TRD a

126 Epistatic interactions between mutations can make evolut

127 e data show the existence of many high-order epistatic interactions between mutations, but also revea

128 intragenic epistasis, we present a survey of epistatic interactions between sequential mutations in T

129 ncolytic properties of r2Reovirus in TNBC to epistatic interactions between the type 3 Dearing M2 gen

130 We further identified 10 epistatic interactions between the vGWAS signals indepen

131 ndscapes were compared and used to calculate epistatic interactions between these mutations and the t

132 as well as provide a rationale to screen for epistatic interactions between variants in IRF6 and RTK

133 Our results demonstrate that these epistatic interactions can be used to prevent the emerge

134 Epistatic interactions can frustrate and shape evolution

135 dies showing that genotype x environment and epistatic interactions control fitness, the influences o

136 actice, however, the vast number of possible epistatic interactions erodes statistical power.

137 measured by fitness effects of mutations and epistatic interactions for TEM-1's original function.

138 Motivated by the problem of learning epistatic interactions from datasets developed in genome

139 Evidence of epistatic interactions has been reported in both humans

140 r, the combinatorial complexity of potential epistatic interactions has severely limited the analysis

141 Investigation of potentially epistatic interactions identified a tufA mutation (Ala27

142 We find epistatic interactions in 67 phenotypes, and in 51 pheno

143 human microglia, we provide new insight into epistatic interactions in AD genes and demonstrate conve

144 n the role of cis-QTLs, trans-QTLs and their epistatic interactions in gene expression.

145 or the full-scale analysis of multiple-locus epistatic interactions in GWAS.

146 We observe that epistatic interactions increase rather than decrease the

147 a finding corroborated by the observation of epistatic interactions involving this complex in vivo.

148 Interpreting epistatic interactions is crucial for understanding evol

149 These results suggest that exploring epistatic interactions is valuable in uncovering the com

150 landscapes due to changes in the fitness and epistatic interactions of some genotypes.

151 ndicating that plasmid-host coevolution, and epistatic interactions on fitness costs are likely to be

152 ns of multiple mutations, possibly involving epistatic interactions or noncoding sequences, have been

153 Epistatic interactions play a fundamental role in molecu

154 uantitative trait loci (QTL) and 24 pairs of epistatic interactions related to yield and yield compon

155 the candidate genes and 75% of the candidate epistatic interactions tested.

156 onal residues comprise a network of strongly epistatic interactions that activate, suppress or reacti

157 in male map showed pleiotropic responses and epistatic interactions with other summer dormant and str

158 We used loss-of-function mutations to define epistatic interactions within the core JA signaling path

159 confounding due to population structure and epistatic interactions, are important to fully explain t

160 f SDS resistance, especially with respect to epistatic interactions, is still unclear.

161 However, directional, epistatic interactions, which reflect regulatory relatio

162 ht be employed to further elucidate relevant epistatic interactions.

163 stical behavior of real sequences induced by epistatic interactions.

164 chloramphenicol reductases revealed complex epistatic interactions.

165 pend on the viral sequence background due to epistatic interactions.

166 s to the topology of fitness landscapes with epistatic interactions.

167 R15 haplotype, or from their combinations or epistatic interactions.

168 computing to detect genome-wide multi-locus epistatic interactions.

169 ich are not shown up in detections of 2-loci epistatic interactions.

170 sed by transformed cells, due to ill-defined epistatic interactions.

171 ic signal, but are less important than other epistatic interactions.

172 ng an avenue for identifying and quantifying epistatic interactions.

173 ters, pairs of variants showed non-additive, epistatic interactions.

174 ent supplemented media, these results reveal epistatic intertwining of metabolism with gene expressio

175 sary for rapid adaptation, as in some highly epistatic landscapes the critical strength does not depe

176 TL mapping identified two additive and three epistatic loci associated with crossover number.

177 en developed for efficient identification of epistatic loci do not systematically exploit linkage dis

178 in the order of millions), identification of epistatic loci is a statistically difficult and computat

179 Epistatic loci that are identified using data from Genom

180 These additive and epistatic loci together explained 24-52% of the phenotyp

181 ular cisplatin and UV hypersensitivity in an epistatic manner with DDB1-DDB2.

182 enotypic manifestation of target genes in an epistatic manner.

183 mical level, genetic level (as assessed with epistatic miniarray profile screens), and phenotypic lev

184 model yeast Schizosaccharomyces pombe Using epistatic miniarray profiles (EMAPs) to survey the genet

185 uble mutant analysis disagreed with a simple epistatic model for HSP90 and AGO1 interaction; rather,

186 ble solution for various biological putative epistatic models in practice.

187 itectures, including additive, dominance and epistatic models.

188 and its targets under additive, dominant and epistatic models.

189 patterns consistent with digenic as well as epistatic modes of inheritance were observed among F(2)

190 We show that epistatic modifiers of the cue polymorphism can evolve t

191 e Procedure for constructing an Additive and Epistatic Multi-Locus model (SPAEML), to detect additive

192 Permissive and restrictive epistatic mutations across the TF-RE interface opened an

193 Victoria virus clades and persisted through epistatic mutations and interclade reassortment-a phenom

194 to decipher and little has been achieved for epistatic mutations, especially at the metabolic level.

195 and other binding partners, due to a set of epistatic mutations.

196 fitness peak is reached via four positively epistatic mutations.

197 of GPSM2 or GNAI function, including in the epistatic Myo15a and Whrn mutants, bundles retain an emb

198 d phosphatases in S. cerevisiae we show that epistatic NEMs can point to modulators of genetic intera

199 Remarkably, this epistatic network of equivalent residues also controls c

200 Here we report the first discovery of an epistatic network of residues that controls the onset of

201 types for multilocus genotype classes in the epistatic networks is often improved by accounting for t

202 Epistatic networks of three SNPs or more influence the e

203 y due to cultural or historical factors than epistatic or environmental constraints.

204 We show that the strongest epistatic pairings from genetic screens of three protein

205 Multi-SNP associations found 102 epistatic pairs associated with traits.

206 We discovered 38 loci and 240 epistatic pairs that influence the minimum inhibitory co

207 Using these experimental epistatic pairs, we compute ab initio folds for a GB1 do

208 ul solution to map multiple QTL with complex epistatic pattern.

209 and stressed the potential importance of the epistatic pleiotropy and of the impact of host living co

210 putation method based on inferring the least epistatic possible sequence-function relationship compat

211 In the third stage, new epistatic QTL are searched in pairs.

212 ond and third stages of analysis for mapping epistatic QTL can be maximized.

213 L is robust and does not bias the search for epistatic QTL due to a genetic property associated with

214 We found that approximately one-half of epistatic QTL overlap regions of residual heterozygosity

215 n impose a significant challenge for finding epistatic QTL reliably.

216 In the second stage, epistatic QTL that interact significantly with other ide

217 re are a number of difficulties for studying epistatic QTL.

218 to 42.33% phenotypic variation (PVE) and 10 epistatic QTLs (E-QTLs) up to 3.31% PVE for oil content

219 Significantly, epistatic QTLs were detected in all datasets.

220 ycle and enucleation deficits are rescued by epistatic reintroduction of either of these 2 EKLF targe

221 This functional conservation of the epistatic relationship between BMP signaling and Blimp-1

222 evated risk of severe disease, suggesting an epistatic relationship between hemoglobin S and PIEZO1 E

223 ion of Pim1 in Deltamrx6 cells, revealing an epistatic relationship between Pim1 and Mrx6.

224 Our findings establish an epistatic relationship between SWI/SNF chromatin remodel

225 uble knockout Fanci-/- Fancd2-/- also showed epistatic relationship for hematological defects while b

226 Thus, the epistatic relationship is context dependent.

227 tory potential of SLP-2 suggest a functional epistatic relationship to Parkin and a protective role o

228 ical phenotype associated with FANCI and the epistatic relationship with FANCD2, we created the first

229 eveloping computational methods for learning epistatic relationships among genetic markers.

230 chanistic effects of different mutations and epistatic relationships among loci that contribute to co

231 on of all pairs of these TFs uncovered their epistatic relationships and highlighted genomic co-local

232 etP (alr2818), asl1930, alr2902, and alr3234 Epistatic relationships between all four genes relating

233 YPOCOTYL IN FAR-RED (HFR1) proteins; and the epistatic relationships between cop1 and pif3, pif4, pif

234 mechanistic modes, and in some cases complex epistatic relationships, exist depending on the signal-d

235 chanistic explanation of their dominance and epistatic relationships.

236 ompromising PPIP5K mutations might extend an epistatic repertoire for XPR1 dysregulation, with pathol

237 that has been successfully used to identify epistatic residues in proteins to infer genomic loci tha

238 d cerebellar cell generation, arguing for an epistatic role of Pals1 in proliferation capacity.

239 a viral protein kinase encoded by HCMV, play epistatic roles in facilitating progression of the viral

240 demonstrating strong evidence of dispersive epistatic selection between populations.

241 gest the operation of other factors, such as epistatic selection, recombination suppression, assortat

242 omponents was originally used to investigate epistatic selection, we demonstrate that values of may a

243 tively corresponding to a selective sweep or epistatic selection.

244 natural variants likely became fixed through epistatic selection.

245 Locus model (SPAEML), to detect additive and epistatic signals simulated using maize and human marker

246 ability to distinguish between additive and epistatic signals, while the number of markers tested di

247 of five SNPs with marginal effects and three epistatic SNP pairs in ARIC-three marginal SNPs were loc

248 ding further elucidation of the additive and epistatic sources contributing to trait variability when

249 The rho and dksA mutations are not epistatic, suggesting they involve different repair path

250 miological studies suggest a polygenetic and epistatic susceptibility model involving the interaction

251 All the epistatic terms involving a particular locus appear in i

252 es, but their effects varied and ranged from epistatic to additive.

253 anthin-biosynthetic operon, crtOPQMN, but is epistatic to alternative sigma factor B.

254 Our analysis demonstrates that tmm-1 is epistatic to atgpi8-1, indicating that either TMM is a G

255 analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of sa

256 A.1 and hta1Delta or hta1-T126A mutants were epistatic to deletion of the Poldelta subunit Pol32, sug

257 i mp mutants are epistatic to Delta mutants and give an additive phenotyp

258 We report that DeltadivIVA mutations are not epistatic to DeltagpsB division-protein mutations in pro

259 ential roles in the release of seed dormancy epistatic to DOG1.

260 ubp7Delta mutants are epistatic to factors involved in histone maintenance and

261 d not protect, replication forks in a manner epistatic to FANCB.

262 Thus, CSF1 is epistatic to FLT1, establishing a link between FLT1 and

263 Brassinosteroid insensitive1 (BRI1) is epistatic to HXK1, as the Glc insensitive2bri1-6 double

264 ant epistasis to loci H and L, whereas H was epistatic to L.

265 Therefore, JAK2 in adipose tissue is epistatic to liver with regard to insulin sensitivity an

266 1 palm1 double mutants revealed that SGL1 is epistatic to LLS1, and LLS1 works with PALM1 in an indep

267 The sae2-S267A mutation is epistatic to mre11-nd for camptothecin (CPT) sensitivity

268 Mutation of slrA was epistatic to mutation of pnpA for the motility-related p

269 ard to nucleotide selectivity, nsp14-ExoN is epistatic to nsp12-RdRp, consistent with its proposed ro

270 TOR was epistatic to PKA components with respect to P-S6.

271 IER5 is epistatic to PPP2R2A, a gene that encodes the PP2A B55al

272 RIN4 pT166 is epistatic to RIN4 pS141.

273 The cca1-1 lhy-20 double mutant is epistatic to sic-3, indicating the LHY and CCA1 splice v

274 n msn2Delta and msn4Delta, but not rpd3, are epistatic to siw14Delta by assessing growth under oxidat

275 Genetic analysis indicates that TGD4 is epistatic to TGD5 in ER-to-plastid lipid trafficking, wh

276 the hierarchy of responses, placing ethylene epistatic to the auxin signaling pathway.

277 e proofreading activity of the nsp14-ExoN is epistatic to the function of the RdRp in fidelity.

278 nce that the crucial female factor rbpms2 is epistatic to the male factor dmrt1 in terms of adult sex

279 , and suggest that the feminizing pathway is epistatic to the masculinizing pathway.

280 r1 (P1; R2R3-MYB transcription factor) to be epistatic to the sm mutation.

281 led lazy1 branch phenotype, indicating it is epistatic to the tac1 shoot phenotype.

282 ether physical (protein-protein) or genetic (epistatic), to study chaperone interaction networks.

283 Epistatic transcriptional profiles mirrored these phenot

284 e SD and SL measurements through main and/or epistatic (two- to four-order interactions) effects.

285 ectively neutral mutations, contributions of epistatic variance are always small.

286 As the magnitude of the epistatic variance depends critically on the heterozygos

287 determining the importance of epistasis and epistatic variance for complex traits, there is consider

288 ethods will be relevant to future studies of epistatic variance in founder populations and crosses.

289 experimental observations of low amounts of epistatic variance in outbred populations are concordant

290 bred populations, which helps in fitting the epistatic variance.

291 , focusing on the potential magnitude of the epistatic variance.

292 cally search for a comprehensive set of such epistatic vulnerabilities.

293 Interestingly, TRAIP is non-epistatic with both NEIL3 and FA pathways in psoralen-IC

294 dph3Delta was epistatic with dph1Delta for sensitivity to hydroxyurea

295 Strikingly, while Paxx loss is epistatic with Ku80, Lig4, and Atm deficiency, Paxx/Xlf

296 ys as groups of genes in which mutations are epistatic with one another or, specifically, "mutually e

297 These genetic defects are epistatic with respect to each other, suggesting that th

298 ip for hematological defects while being not epistatic with respect to generating viable mice in cros

299 suggestion we found that REV1 and FANCD2 are epistatic with respect to sensitivity to the double-stra

300 rsensitivity, and the gene encoding RNF4 was epistatic with the other genes encoding members of the F