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EGR4 is critical for cell-fate determination and maintenance of Geniculate Ganglion neurons underlying sweet and umami taste

ABSTRACT: EGR4 is critical for cell-fate determination and maintenance of Geniculate Ganglion neurons underlying sweet and umami taste

PROVIDER: PRJNA927497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23229687_1.fastq.gz	Fastqsanger.gz
	SRR23229687_2.fastq.gz	Fastqsanger.gz
	SRR23229688_1.fastq.gz	Fastqsanger.gz
	SRR23229688_2.fastq.gz	Fastqsanger.gz
	SRR23229689_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

EGR4 is critical for cell-fate determination and maintenance of Geniculate Ganglion neurons underlying sweet and umami taste

Project description:The sense of taste starts with activation of receptor cells in taste buds by chemical stimuli which then communicate this signal via innervating oral sensory neurons to the CNS. The cell bodies of oral sensory neurons reside in the geniculate ganglion (GG) and nodose/petrosal/jugular ganglion. The geniculate ganglion contains two main neuronal populations, BRN3A+ somatosensory neurons that innervate the pinna, and PHOX2B+ sensory neurons that innervate the oral cavity. While much is known about the different taste bud cell subtypes, much less is known about the molecular identities of PHOX2B+ sensory subpopulations. In the GG as many as 12 different subpopulations have been predicted from electrophysiological studies, while transcriptional identities exist for only 3-6. Importantly, the cell fate pathways that diversify PHOX2B+ oral sensory neurons into these subpopulations are unknown. The transcription factor EGR4 was identified as being highly expressed in GG neurons. EGR4 deletion causes GG oral sensory neurons to lose their expression of PHOX2B and other oral sensory genes, and upregulate BRN3A. This is followed by a severe loss of chemosensory innervation of taste buds, a loss of Type II taste cells responsive to bitter, sweet, and umami stimuli, and a concomitant increase in Type I glial-like taste bud cells. These deficits culminate in a loss of nerve responses to sweet and umami taste qualities. Taken together, we identify a critical role of EGR4 in cell fate specification and maintenance of subpopulations of GG neurons, which in turn maintain the appropriate sweet and umami taste receptor cells.

2023-02-01 | GSE223724 | GEO

Single-cell RNA-Seq of the geniculate ganglion from Mus musculus

Project description:We use comprehensive and unsupervised transcriptome analyses to provide molecular classifications of sensory neurons in the mouse geniculate ganglion. 96 neurons were isolated on a C1 Fluodigm chip, underwent RNA-Seq, and iteratively clustered into sub-classes.

2017-10-02 | GSE102443 | GEO

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

| PRJNA609758 | ENA

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

| PRJNA609759 | ENA

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

| PRJNA609755 | ENA

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

| PRJNA609724 | ENA

Selection of the dimeric sweet taste receptor for surface expression and intersubunit interactions

Project description:The sweet taste receptor is a heterodimer of two class C G protein-coupled receptors (GPCRs), T1R2 and T1R3. While homologous structures of individual domains have been determined, the architecture of the full length T1R2-T1R3 dimer is unknown. Using random mutagenesis and cell sorting, we identify single point mutations and a C-terminal intracellular retention motif in human T1R2 that modulate surface expression and co-trafficking with T1R3 in a HEK293-derivative cell line. A comprehensive mutational scan of T1R2 based on surface expression of both subunits revealed conserved sites for T1R3 interactions, including surfaces on lobe 1 of the ligand binding domain, cysteine rich domain, and transmembrane helix 6. Using the mutational scan to guide modeling of the T1R2-T1R3 dimer predicts a twisted architecture that can explain how outwards motion of lobes 2 in the ligand-binding domains is translated into reorganization of transmembrane regions, and further predicts that extracellular loops 2 form continuous folded structures with the cysteine-rich domains near the dimer axis. These insights into the putative structural organization of the human sweet taste receptor have general implications for the mechanism of class C GPCRs.

2018-12-01 | GSE115751 | GEO

Altered learning, memory, and social behavior in type 1 taste receptor subunit 3 knock-out mice are associated with neuronal dysfunction.

Project description:The type 1 taste receptor member 3 (T1R3) is a G protein-coupled receptor involved in sweet-taste perception. Besides the tongue, the T1R3 receptor is highly expressed in brain areas implicated in cognition, including the hippocampus and cortex. As cognitive decline is often preceded by significant metabolic or endocrinological dysfunctions regulated by the sweet-taste perception system, we hypothesized that a disruption of the sweet-taste perception in the brain could have a key role in the development of cognitive dysfunction. To assess the importance of the sweet-taste receptors in the brain, we conducted transcriptomic and proteomic analyses of cortical and hippocampal tissues isolated from T1R3 knock-out (T1R3KO) mice. The effect of an impaired sweet-taste perception system on cognition functions were examined by analyzing synaptic integrity and performing animal behavior on T1R3KO mice. Although T1R3KO mice did not present a metabolically disrupted phenotype, bioinformatic interpretation of the high-dimensionality data indicated a strong neurodegenerative signature associated with significant alterations in pathways involved in neuritogenesis, dendritic growth, and synaptogenesis. Furthermore, a significantly reduced dendritic spine density was observed in T1R3KO mice together with alterations in learning and memory functions as well as sociability deficits. Taken together our data suggest that the sweet-taste receptor system plays an important neurotrophic role in the extralingual central nervous tissue that underpins synaptic function, memory acquisition, and social behavior.

2017-05-17 | GSE97677 | GEO

The single-cell RNA sequencing for α-gustducin-positive taste cells

Project description:Taste buds are complex sensory organs that are embedded in the epithelium of fungiform papillae (FP) and circumvallate papillae (CV). The sweet, bitter, and umami taste are sensed by type II taste cells that expressed taste receptors (Tas1rs and Tas2rs) which coupled with taste G-protein α-gustducin. Recent studies revealed that the taste response profiles of α-gustducin-expressing cells are different between FP and CV. We applied the high-throughput single-cell RNA-sequencing combined with fluorescence-activated cell sorting (FACS) to profile the transcriptome of the α-gustducin-expressing taste cells in both fungiform and circumvallatae papillae with transgenic mice expressing green fluorescent protein (GFP).

2021-08-01 | GSE169191 | GEO

High Sox2 expression predicts taste lineage competency of lingual progenitors in vitro

Project description:Taste buds on the tongue are collections of taste receptor cells (TRCs) that detect sweet, sour, salty, umami and bitter stimuli. Like non-taste lingual epithelium, TRCs are renewed from basal keratinocytes, many of which express the transcription factor SOX2. Genetic lineage tracing has shown SOX2+ lingual progenitors give rise to both taste and non-taste lingual epithelium in the posterior circumvallate taste papilla (CVP) of mice. However, SOX2 is variably expressed among CVP cells suggesting that their progenitor potential may vary. Using transcriptome analysis and organoid technology, we show highly expressing SOX2+ cells are taste-competent progenitors that give rise to organoids comprising both TRCs and lingual epithelium, while organoids derived from low-expressing SOX2+ progenitors are composed entirely of non-taste cells. Hedgehog and WNT/ß-catenin are required for taste homeostasis in adult mice, but only WNT/ß-catenin promotes TRC differentiation in vitro and does so only in organoids derived from higher SOX2+ taste lineage-competent progenitors.

2023-02-07 | GSE207624 | GEO

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