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Its prevalence is ~5% in German\u2010speaking individuals. Although the etiology of dyslexia largely remains to be determined, comprehensive evidence supports deficient phonological processing as a major contributing factor. An important prerequisite for phonological processing is auditory discrimination and, thus, essential for acquiring reading and spelling skills. The event\u2010related potential Mismatch Response (<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>) is an indicator for auditory discrimination capabilities with dyslexics showing an altered late component of<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>in response to auditory input.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this study, we comprehensively analyzed associations of dyslexia\u2010specific late<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>s with genetic variants previously reported to be associated with dyslexia\u2010related phenotypes in multiple studies comprising 25 independent single\u2010nucleotide polymorphisms (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s) within 10 genes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>First, we demonstrated validity of these<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s for dyslexia in our sample by showing that additional inclusion of a polygenic risk score improved prediction of impaired writing compared with a model that used<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>alone. Secondly, a multifactorial regression analysis was conducted to uncover the subset of the 25<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s that is associated with the dyslexia\u2010specific late component of<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>. In total, four independent<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s within<jats:italic><jats:styled-content style=\"fixed-case\">DYX<\/jats:styled-content>1C1<\/jats:italic>and<jats:italic><jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>2C<\/jats:italic>2 were found to be associated with<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>stronger than expected from multiple testing. To explore potential pathomechanisms, we annotated these variants with functional data including tissue\u2010specific expression analysis and<jats:styled-content style=\"fixed-case\">eQTL<\/jats:styled-content>s.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings corroborate the late component of<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>as a potential endophenotype for dyslexia and support tripartite relationships between dyslexia\u2010related<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s, the late component of<jats:styled-content style=\"fixed-case\">MMR<\/jats:styled-content>and dyslexia.<\/jats:p><\/jats:sec>","DOI":"10.1002\/brb3.851","type":"journal-article","created":{"date-parts":[[2017,10,18]],"date-time":"2017-10-18T07:42:37Z","timestamp":1508312557000},"source":"Crossref","is-referenced-by-count":8,"title":["<i><scp>ATP<\/scp>2C2<\/i>and<i><scp>DYX<\/scp>1C1<\/i>are putative modulators of 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