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Runx1 controls auditory sensory neuron diversity in mice
Brikha R Shrestha1, Lorna Wu2, Lisa V Goodrich2
1Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA; Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, MA 02114, USA; Department of Otolaryngology, Harvard Medical School, Boston, MA 02114, USA.
Developmental Cell
|February 21, 2023
Summary
The transcription factor Runx1 is crucial for developing specific auditory neuron subtypes in mice. Its absence causes more neurons to adopt a general sound-sensing (Ia) identity, impacting auditory coding.
Area of Science:
- Neuroscience
- Developmental Biology
- Auditory System Research
Background:
- Spiral ganglion neurons (SGNs) in mice encode sound via three distinct subtypes: Ia, Ib, and Ic.
- Understanding the molecular mechanisms that establish and maintain these SGN subtypes is critical for auditory neuroscience.
Purpose of the Study:
- To investigate the role of the transcription factor Runx1 in determining the subtype composition of spiral ganglion neurons.
- To explore the plasticity of SGN identities during postnatal development.
Main Methods:
- Utilized mouse models with targeted deletion of the Runx1 gene (Runx1CKO) during embryonic and postnatal development.
- Analyzed SGN subtype identity through gene expression related to neuronal function and connectivity.
- Assessed functional properties of SGNs and their synapses using electrophysiological recordings.
Main Results:
- Runx1 is essential for the proper differentiation of Ib and Ic SGN subtypes, being enriched in their precursors.
- Loss of Runx1 leads to a conversion of SGNs towards the Ia subtype identity, affecting both gene expression and synaptic properties.
- Runx1 deletion postnatally also induced SGN identity plasticity, redirecting Ib/Ic neurons to Ia identity.
Conclusions:
- Runx1 acts as a key regulator controlling the hierarchical development and subtype specification of spiral ganglion neurons.
- Auditory neuron identities are not fixed and exhibit significant plasticity during postnatal development, offering potential avenues for therapeutic interventions.
