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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 (CKO)

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Runx1 controls auditory sensory neuron diversity in mice.

Project description: Not available

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Olfactory Sensory Neuron Diversity Beyond OR Genes in mice

Project description:Olfactory Sensory Neuron Diversity Beyond OR Genes in mice

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Olfactory Sensory Neuron Diversity Beyond OR Genes in mice [scRNAseq]

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Olfactory Sensory Neuron Diversity Beyond OR Genes in mice [scATACseq]

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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.

2020-04-01 | GSE140883 | GEO

SIX1 is required for adult cochlear sensory epithelium homeostasis and auditory function

Project description:The mammalian auditory sensory epithelium consists of luminal hair cells (HCs), whose stereociliary bundles convert sound vibrations into electrical signals, and basal supporting cells (SCs), which provide mechanical stability and homeostasis. During development, the transcription factor SIX1 specifies otic epithelial cells into neurosensory progenitors and commits progenitors to the HC lineage, but its contribution after birth has remained elusive. Here we show that SIX1 is essential for maintaining the structure and function of the sensory epithelium in the adult cochlea. Conditional deletion of Six1 in SCs, inner HCs, or outer HCs of 5–6-week-old mice results in profound deafness. SC-specific deletion causes rapid SC loss followed by secondary HC degeneration, whereas Six1 loss in inner or outer HCs disrupts stereociliary-bundle architecture and leads to progressive HC death. To uncover the underlying regulatory circuitry, we mapped genome-wide SIX1 occupancy in the mature cochlea. SIX1 binds DNA elements/enhancers near genes involved in cell adhesion, junctional integrity, actin dynamics, hair-bundle assembly, ion-channel, mechanotransduction, and cell survival, many of which are frequently mutated in hereditary deafness. Motif analysis showed that these SIX1-bound sites retain the core co-motifs found in SIX1 peaks in embryonic cochlea, suggesting reuse of embryonic cofactors. Notably, SIX1 occupies an intronic enhancer of Srf and physically interacts with SRF protein, positioning SIX1 atop an SRF-centered actin-cytoskeletal circuit crucial for bundle stability. Together, our findings redefine SIX1 as a lifelong regulator of cochlear homeostasis and reveal its downstream networks that maintain the adult auditory sensory epithelium.

2026-07-16 | GSE303887 | GEO

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