ArticleCerebral cortex (New York, N.Y. : 1991)2017
Knockout Mice for Dyslexia Susceptibility Gene Homologs KIAA0319 and KIAA0319L have Unaffected Neuronal Migration but Display Abnormal Auditory Processing.
Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Hypothesis-driven genome-wide association studies provide novel insights into genetics of reading disabilities.Translational psychiatry · 2022Pooled it
- Innovative Method for Fully Automated, Enzyme-Free Tissue Dissociation and Preparation for Single-Cell Analysis.Cellular and molecular bioengineering · 2025Article
- AAVR Expression is Essential for AAV Vector Transduction in Sensory Hair Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Genetic Modifications of Developmental Dyslexia and Its Representation Using In Vivo, In Vitro Model.Global medical genetics · 2024Review
- Hardwiring tissue-specific AAV transduction in mice through engineered receptor expression.Nature methods · 2023Article
- Rapid auditory processing and medial geniculate nucleus anomalies in Kiaa0319 knockout mice.Genes, brain, and behavior · 2022Article
- Animal models of developmental dyslexia.Frontiers in neuroscience · 2022Review
- The dyslexia susceptibility KIAA0319 gene shows a specific expression pattern during zebrafish development supporting a role beyond neuronal migration.The Journal of comparative neurology · 2019Article
- Neuroinflammation mediates noise-induced synaptic imbalance and tinnitus in rodent models.PLoS biology · 2019Article
- The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on.The European journal of neuroscience · 2018Review
- AU040320 deficiency leads to disruption of acrosome biogenesis and infertility in homozygous mutant mice.Scientific reports · 2018Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Developmental dyslexia is a neurodevelopmental disorder that affects reading ability caused by genetic and non-genetic factors. Amongst the susceptibility genes identified to date, KIAA0319 is a prime candidate. RNA-interference experiments in rats suggested its involvement in cortical migration but we could not confirm these findings in Kiaa0319-mutant mice. Given its homologous gene Kiaa0319L (AU040320) has also been proposed to play a role in neuronal migration, we interrogated whether absence of AU040320 alone or together with KIAA0319 affects migration in the developing brain. Analyses of AU040320 and double Kiaa0319;AU040320 knockouts (dKO) revealed no evidence for impaired cortical lamination, neuronal migration, neurogenesis or other anatomical abnormalities. However, dKO mice displayed an auditory deficit in a behavioral gap-in-noise detection task. In addition, recordings of click-evoked auditory brainstem responses revealed suprathreshold deficits in wave III amplitude in AU040320-KO mice, and more general deficits in dKOs. These findings suggest that absence of AU040320 disrupts firing and/or synchrony of activity in the auditory brainstem, while loss of both proteins might affect both peripheral and central auditory function. Overall, these results stand against the proposed role of KIAA0319 and AU040320 in neuronal migration and outline their relationship with deficits in the auditory system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.