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Runx1 Controls Auditory Sensory Neuron Diversity (iCKO)

ABSTRACT: Runx1 Controls Auditory Sensory Neuron Diversity (iCKO)

PROVIDER: PRJNA864782 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20730575.fastq.gz	Fastqsanger.gz
	SRR20730576.fastq.gz	Fastqsanger.gz

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Runx1 Controls Auditory Sensory Neuron Diversity (CKO)

Project description:Runx1 Controls Auditory Sensory Neuron Diversity (CKO)

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Runx1 Controls Auditory Sensory Neuron Diversity (iCKO)

Project description:As the primary sensory neurons of the auditory system, Type I spiral ganglion neurons (SGNs) encode sound stimulus properties critical for the formation of auditory percept in higher brain areas. Their functional heterogeneity is thought to contribute to our ability to hear a wide range of sound intensities and against background noise, but how SGN diversity arises during development is poorly understood. Here we studied the role of the transcription factor Runx1 in establishing SGN heterogeneity in the mouse cochlea by single cell RNA-sequencing.

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Runx1 controls auditory sensory neuron diversity in mice.

Project description:Sound stimulus is encoded in mice by three molecularly and physiologically diverse subtypes of sensory neurons, called Ia, Ib, and Ic spiral ganglion neurons (SGNs). Here, we show that the transcription factor Runx1 controls SGN subtype composition in the murine cochlea. Runx1 is enriched in Ib/Ic precursors by late embryogenesis. Upon the loss of Runx1 from embryonic SGNs, more SGNs take on Ia rather than Ib or Ic identities. This conversion was more complete for genes linked to neuronal function than to connectivity. Accordingly, synapses in the Ib/Ic location acquired Ia properties. Suprathreshold SGN responses to sound were enhanced in Runx1CKO mice, confirming the expansion of neurons with Ia-like functional properties. Runx1 deletion after birth also redirected Ib/Ic SGNs toward Ia identity, indicating that SGN identities are plastic postnatally. Altogether, these findings show that diverse neuronal identities essential for normal auditory stimulus coding arise hierarchically and remain malleable during postnatal development.

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Molecular diversity of auditory critical period plasticity revealed by single-nucleus RNA sequencing

Project description:Auditory experience drives neural circuit refinement during auditory circuit development, but little is known about the genetic regulation of this developmental process. The primary auditory cortex (A1) exhibits a critical period for thalamocortical connectivity between postnatal days P12 and P15, during which tone exposure alters the tonotopic topography of A1. We hypothesized that a coordinated, multicellular transcriptional program governs this window for patterning of the auditory cortex. To test this idea, we generated a multicellular map of gene expression by performing droplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points spanning the tonotopic critical period (P10, P15, P20). We also tone-reared mice (7 kHz pips) during the 3-day critical period and carried out snRNA-seq of A1 at P15 and P20. Using semi-supervised clustering and marker genes, we identified and profiled neuronal (glutamatergic and GABAergic) and non-neuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types in A1 under these different conditions to identify candidate genes that might regulate auditory critical period plasticity. By comparing normally reared and tone-reared mice, we identified hundreds of genes in both glutamatergic and GABAergic cells with altered expression as a result of sensory manipulation in the critical period. In addition, we identified previously unknown effects of developmental tone exposure on interneuron developmental trajectories. This single-cell transcriptomic resource of the developing auditory cortex will provide a powerful discovery platform for future characterization of mediators of tonotopic plasticity.

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Project description:Profiling Kif5A RNA targets in sensory neuron axons

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