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ISL1 is necessary for auditory neuron development and contributes toward tonotopic organization
Journal article   Open access   Peer reviewed

ISL1 is necessary for auditory neuron development and contributes toward tonotopic organization

Iva Filova, Kateryna Pysanenko, Mitra Tavakoli, Simona Vochyanova, Martina Dvorakova, Romana Bohuslavova, Ondrej Smolik, Valeria Fabriciova, Petra Hrabalova, Sarka Benesova, …
Proceedings of the National Academy of Sciences - PNAS, Vol.119(37), pp.e2207433119-e2207433119
09/13/2022
DOI: 10.1073/pnas.2207433119
PMCID: PMC9478650
PMID: 36074819
url
https://doi.org/10.1073/pnas.2207433119View
Published (Version of record) Open Access

Abstract

A cardinal feature of the auditory pathway is frequency selectivity, represented in a tonotopic map from the cochlea to the cortex. The molecular determinants of the auditory frequency map are unknown. Here, we discovered that the transcription factor ISL1 regulates the molecular and cellular features of auditory neurons, including the formation of the spiral ganglion and peripheral and central processes that shape the tonotopic representation of the auditory map. We selectively knocked out Isl1 in auditory neurons using Neurod1Cre strategies. In the absence of Isl1, spiral ganglion neurons migrate into the central cochlea and beyond, and the cochlear wiring is profoundly reduced and disrupted. The central axons of Isl1 mutants lose their topographic projections and segregation at the cochlear nucleus. Transcriptome analysis of spiral ganglion neurons shows that Isl1 regulates neurogenesis, axonogenesis, migration, neurotransmission-related machinery, and synaptic communication patterns. We show that peripheral disorganization in the cochlea affects the physiological properties of hearing in the midbrain and auditory behavior. Surprisingly, auditory processing features are preserved despite the significant hearing impairment, revealing central auditory pathway resilience and plasticity in Isl1 mutant mice. Mutant mice have a reduced acoustic startle reflex, altered prepulse inhibition, and characteristics of compensatory neural hyperactivity centrally. Our findings show that ISL1 is one of the obligatory factors required to sculpt auditory structural and functional tonotopic maps. Still, upon Isl1 deletion, the ensuing central plasticity of the auditory pathway does not suffice to overcome developmentally induced peripheral dysfunction of the cochlea.

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