Abstract
Replying to A. R. Wood et al. Nature 514, 10.1038/nature13691 (2014).
We thank Wood et al.1 for their interesting observations and although their proposed mechanism does not explain all our reported results, we acknowledge that alternative mechanisms could be behind the observation of epistatic signals. Although we replicate our results in large, independent samples, 19/30 of our reported interactions (Table 1 in ref. 2), Wood et al.1 do not replicate in the InCHIANTI data set (n = 450) at a type-I error rate of 0.05/30 = 0.002, including none of our reported cis–trans interactions. Having insufficient data to replicate the discovery interactions makes it problematic to draw firm conclusions on the reported cis–trans effects.
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References
Wood, A. R. et al. Another explanation for apparent epistasis. Nature 514, http://dx.doi.org/10.1038/nature13691 (2014)
Hemani, G. et al. Detection and replication of epistasis influencing transcription in humans. Nature 508, 249–253 (2014)
Westra, H. J. et al. Systematic identification of trans eQTLs as putative drivers of known disease associations. Nature Genet. 45, 1238–1243 (2013)
Powell, J. E. et al. Congruence of additive and non-additive effects on gene expression estimated from pedigree and SNP data. PLoS Genet. 9, e1003502 (2013)
Powell, J. E. et al. The Brisbane Systems Genetics Study: genetical genomics meets complex trait genetics. PLoS ONE 7, e35430 (2012)
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Hemani, G., Shakhbazov, K., Westra, HJ. et al. Hemani et al. reply. Nature 514, E5–E6 (2014). https://doi.org/10.1038/nature13692
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DOI: https://doi.org/10.1038/nature13692
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