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Persistent Epigenetic Reprogramming of Sweet Taste by Diet

ABSTRACT: Persistent Epigenetic Reprogramming of Sweet Taste by Diet

PROVIDER: PRJNA609759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11215685_1.fastq.gz	Fastqsanger.gz
	SRR11215685_2.fastq.gz	Fastqsanger.gz
	SRR11215686_1.fastq.gz	Fastqsanger.gz
	SRR11215686_2.fastq.gz	Fastqsanger.gz
	SRR11215687_1.fastq.gz	Fastqsanger.gz

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Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

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Persistent Epigenetic Reprogramming of Sweet Taste by Diet

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Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:Persistent Epigenetic Reprogramming of Sweet Taste by Diet

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Persistent epigenetic reprogramming of sweet taste by diet.

Project description:Diets rich in sugar, salt, and fat alter taste perception and food preference, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of Drosophila melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.

| S-EPMC7673743 | biostudies-literature

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-11 | GSE146245 | GEO

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:We report the application of targeted DNA Adenine Methyltransferase identification DNA sequencing technology for high-throughput profiling of Pcl occupancy in the Gr5a cells of male Drosophila melanogaster adults. By expressing the UAS-LT3-Dam::Pcl and UAS-LT3-Dam transgene using the Gr5a-GAL4;tubulinGAL80ts driver.

2020-11-11 | GSE146242 | GEO

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:We report the application of ribosomal profiling based RNA sequencing technology for high-throughput profiling of the Gr5a cells of male Drosophila melanogaster adults. By expressing the UAS-Rpl3-3XFLAG transgene using the Gr5a-GAL4 driver on Pclc429 mutant flies.

2020-11-11 | GSE146241 | GEO

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

2020-11-11 | GSE146214 | GEO

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

Geometric Framework for nutrition on Sucrose Taste Sensitization in Drosophila

Project description:Numerous studies show dietary carbohydrates (C) affect the sensation of sweetness. However, protein (P) is one of the most critical macronutrients in the diet as well. It is still unclear how carbohydrates and proteins interact to influence sweet taste sensitivity. Here, we use the nutritional geometry framework (NGF) to tackle this problem in Drosophila melanogaster. Our results showed that the combination of high protein and low carbohydrates caused higher taste responses to sucrose stimuli in both sexes. Additionally, transcriptome analysis revealed that the gene expression of glycine, serine, and threonine pathway in the high-protein, low-carbohydrate diet was significantly upregulated, compared to a diet with low protein, and high carbohydrate. We confirmed that serine and threonine supplementation in the high-carbohydrate, low-protein diet enhanced the sucrose sensitivity of flies. Our results demonstrate that sucrose taste sensitivity is affected by the dietary balance of protein and carbohydrates possibly mediated by the change in serine, and threonine. The high protein, low carbohydrate diets enhanced sucrose taste sensitivity.

2023-02-16 | GSE217385 | GEO

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