Onset of taste cell renewal starts at birth and coincides with a shift in SHH function
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA670917 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12884055.fastq.gz | Fastqsanger.gz | |||
| SRR12884056.fastq.gz | Fastqsanger.gz |
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Project description:RNAseq was employed to profile taste progenitors (SOX2-GFPhigh) and non-taste epithelial progenitors (SOX2-GFPlow) at the onset of taste cell renewal at birth. This dataset was acquired via FACS of SOX2-GFP+ epithelial cells from SOX2gfp/+ mouse pups at P0.
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Project description:Embryonic taste bud primordia are specified as taste placodes on the tongue surface and differentiate into the first taste receptor cells (TRCs) at birth. Throughout adult life, TRCs are continually regenerated from epithelial progenitors. Sonic hedgehog (SHH) signaling regulates TRC development and renewal, repressing taste fate embryonically, but promoting TRC differentiation in adults. Here, using mouse models, we show TRC renewal initiates at birth and coincides with onset of SHHs pro-taste function. Using transcriptional profiling to explore molecular regulators of renewal, we identified Foxa1 and Foxa2 as potential SHH target genes in lingual progenitors at birth and show that SHH overexpression in vivo alters FoxA1 and FoxA2 expression relevant to taste buds. We further bioinformatically identify genes relevant to cell adhesion and cell locomotion likely regulated by FOXA1;FOXA2 and show that expression of these candidates is also altered by forced SHH expression. We present a new model where SHH promotes TRC differentiation by regulating changes in epithelial cell adhesion and migration.
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Project description:Taste stem/progenitor cells from the mouse posterior tongue have been recently used to generate taste bud organoids. However, the inaccessible location of the taste receptor cells is observed in conventional organoids. Here, we established a suspension culture method for fine tuning of taste bud organoid by apicobasal polarity alteration to form the accessible localization of taste receptor cells in organoid. Compared to conventional Matrigel-embedded organoids, suspension-cultured organoids showed comparable differentiation and renewal rates to those of taste buds in vivo and exhibited functional taste receptor cells and cycling progenitor cells. Accessible taste receptor cells on the outer region of taste bud organoids enabled the direct application of calcium imaging for evaluating the taste response. Moreover, suspension-cultured organoids could be genetically altered using gene editing methods. Suspension-cultured taste bud organoid harmoniously integrated with the recipient lingual epithelium; maintained the taste receptor cells and gustatory innervation capacity. Thus, we propose that suspension-cultured organoids may provide efficient model for taste research including taste bud development, regeneration and transplantation
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Project description:To uncover novel molecules involved in taste detection, we performed a microarray-based screen for genes enriched in taste neurons. Proboscis RNA from flies homozygous for a recessive poxn null mutation was compared to RNA from heterozygous controls. Poxn mutants have a transformation of labellar gustatory chemosensory bristles into mechanosensory bristles and therefore lack most or all taste neurons. Experiment Overall Design: Proboscises of poxn70 homozygous mutant and poxn70 heterozygous mutant males (8-18 days post eclosure) were dissected, and total RNA was harvested in Trizol according to standard trizol protocol. Samples for each microarray were prepared from 164-280 proboscises. We performed 3 biological replicates for each genotype.
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Project description:To understand the mechanisms that regulate the renewal and maintenance of taste cells we performed RNA-sequencing analysis on isolated taste cells from 2 and 6 month old mice to determine how alterations in the taste cell-transcriptome regulate taste cell maintenance and function in adults. We found that the Activator Protein-1 (AP1) transcription factors (c-Fos, Fosb and c-Jun) and genes associated with this pathway were significantly downregulated in taste cells from 6 month old mice and further declined at 12 months. We generated conditional c-Fos- knockout mice to target K14-expressing cells, including differentiating taste cells. c-Fos deletion caused a severe perturbation in taste bud structure and resulted in a significant reduction in the taste bud size. c-Fos deletion also affected taste cell turnover as evident by, a decrease in proliferative markers, and upregulation of the apoptotic marker cleaved-PARP. Thus, AP1 factors are important regulators of adult taste cell renewal and their downregulation negatively impacts taste maintenance. Comparison of genes responsible for peripheral Taste system maintenance at age, 3 and 6 months. processed_data.txt: List of B vs S gene expression data gene_exp.diff: cuffdiff data for 2 and 6 month taste cells
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