Investigating the role of the dyslexia susceptibility gene KIAA0319 in zebra finch auditory perception 131 views

Developmental dyslexia is a common learning disorder that affects approximately 10% of the population and results in a marked decrease in phoneme processing, suggesting an underlying deficit in auditory processing. Dyslexia is associated with loss-of-function mutations in KIAA0319 (Galaburda et al., 2006), but the function of this gene remains poorly understood. Reduced KIAA0319 expression in rodents results in electrophysiological and behavioral auditory deficits (Centanni et al., 2014). I hypothesize that KIAA0319 may play a role in experience-dependent plasticity of intrinsic neuronal dynamics during phonetic learning. Like humans, zebra finches grow up in complex acoustical environments and learn how to recognize conspecific vocalizations during an early sensitive period, which makes them a useful model to test this hypothesis. To test for a causal role in this plasticity, I developed adeno-associated viruses (AAVs) carrying short-hairpin ribonucleic acid (shRNA) constructs targeting KIAA0319. This approach allowed me to investigate whether the developmental knockdown of KIAA0319 impairs song learning, alters intrinsic plasticity, and modulates the expression of other proteins implicated in neuronal plasticity. Additionally, I made and characterized an anti-KIAA0319 antibody to confirm knockdown of KIAA0319 in zebra finches. The antibody demonstrated specificity in vitro, but knockdown was not confirmed in vivo, which limits any interpretation of the behavioral data. Future work should combine mass spectrometry, co-immunoprecipitation, and confirm in vivo knockdown to more directly test KIAA0319's role in auditory learning.

PHD (Doctor of Philosophy)

English

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2026-07-30