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Although underlying biological and genetic mechanisms remain unclear, anomalies in phonological processing and auditory processing have been associated with dyslexia. Several candidate risk genes have also been identified, with <jats:italic>KIAA0319<\/jats:italic> as a main candidate. Animal models targeting the rodent homolog (<jats:italic>Kiaa0319<\/jats:italic>) have been used to explore putative behavioral and anatomic anomalies, with mixed results. For example after downregulation of <jats:italic>Kiaa0319<\/jats:italic> expression in rats via shRNA, significant adult rapid auditory processing impairments were reported, along with cortical anomalies reflecting atypical neuronal migration. Conversely, <jats:italic>Kiaa0319<\/jats:italic> knockout (KO) mice were reported to have typical adult auditory processing, and no visible cortical anomalies. To address these inconsistencies, we tested <jats:italic>Kiaa0319<\/jats:italic> KO mice on auditory processing tasks similar to those used previously in rat shRNA knockdown studies. Subsequent neuroanatomic analyses on these same mice targeted medial geniculate nucleus (MGN), a receptive communication\u2010related brain structure. Results confirm that <jats:italic>Kiaa0319<\/jats:italic> KO mice exhibit significant auditory processing impairments specific to rapid\/brief stimuli, and also show significant volumetric reductions and a shift toward fewer large and smaller neurons in the MGN. The latter finding is consistent with post mortem MGN data from human dyslexic brains. Combined evidence supports a role for <jats:italic>KIAA0319<\/jats:italic> in the development of auditory CNS pathways subserving rapid auditory processing functions critical to the development of speech processing, language, and ultimately reading. Results affirm <jats:italic>KIAA0319<\/jats:italic> variation as a possible risk factor for dyslexia specifically via anomalies in central acoustic processing pathways.<\/jats:p>","DOI":"10.1111\/gbb.12808","type":"journal-article","created":{"date-parts":[[2022,4,14]],"date-time":"2022-04-14T01:58:35Z","timestamp":1649901515000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Rapid auditory processing and medial geniculate nucleus anomalies in <i>Kiaa0319<\/i> knockout mice"],"prefix":"10.1111","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6849-6757","authenticated-orcid":false,"given":"Peter A.","family":"Perrino","sequence":"first","affiliation":[{"name":"Department of Psychological Science\/Behavioral Neuroscience University of Connecticut  Storrs Connecticut USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6911-3845","authenticated-orcid":false,"given":"Renee Y.","family":"Chasse","sequence":"additional","affiliation":[{"name":"Department of Psychological Science\/Behavioral Neuroscience University of Connecticut  Storrs Connecticut USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony P.","family":"Monaco","sequence":"additional","affiliation":[{"name":"Office of the President Tufts University  Medford Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zolt\u00e1n","family":"Moln\u00e1r","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy, and Genetics University of Oxford  Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7717-4477","authenticated-orcid":false,"given":"Antonio","family":"Velayos\u2010Baeza","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy, and Genetics University of Oxford  Oxford UK"},{"name":"Wellcome Centre for Human Genetics University of Oxford  Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1748-9506","authenticated-orcid":false,"given":"R. 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