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Altering metabolism to program cell identity via NAD+ dependent deacetylation [RNA-seq]

ABSTRACT: Altering metabolism to program cell identity via NAD+ dependent deacetylation [RNA-seq]

PROVIDER: PRJNA725905 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14351852.fastq.gz	Fastqsanger.gz
	SRR14351853.fastq.gz	Fastqsanger.gz
	SRR14351854.fastq.gz	Fastqsanger.gz
	SRR14351855.fastq.gz	Fastqsanger.gz
	SRR14351856.fastq.gz	Fastqsanger.gz

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Altering metabolism to program cell identity via NAD+ dependent deacetylation

Project description:Altering metabolism to program cell identity via NAD+ dependent deacetylation

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Altering metabolism to program cell identity via NAD+ dependent deacetylation [ATAC-seq]

Project description:Altering metabolism to program cell identity via NAD+ dependent deacetylation [ATAC-seq]

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Altering metabolism programs cell identity via NAD+ dependent deacetylation

Project description:Cells change their metabolic profiles in response to an underling gene regulatory network, but how can alterations in metabolism encode specific transcriptional instructions? Here we show that forcing metabolic change in embryonic stem cells (ESCs) promotes a developmental identity that better approximates the inner cell mass (ICM) of the mammalian blastocyst in cultures we refer to as enhanced metabolic ESCs (EMESCs). The creation of EMESCs depends on the inhibition of glycolysis and stimulation of oxidative phosphorylation (OXPHOS), that in turns activates NAD+-dependent deacetlylases of the Sirtuin family. The activation of this pathway leads to the deacetylation of histones and key transcription factors leading to a revised ICM-like gene regulatory network. The exploitation of the NAD+/NADH coenzyme normally coupled to elevated OXPHOS to program lineage specific transcription suggests new paradigms for how cells respond to alterations in their environment.

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Altering metabolism to program cell identity via NAD+ dependent deacetylation [ATAC-seq]

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Altering metabolism programs cell identity via NAD+-dependent deacetylation [CUT&Tag]

Project description:Altering metabolism programs cell identity via NAD+-dependent deacetylation [CUT&Tag]

| PRJNA1060259 | ENA

Altering metabolism programs cell identity via NAD+-dependent deacetylation [CUT&Tag]

Project description:Cells change their metabolic profiles in response to underlying gene regulatory networks, but how can alterations in metabolism encode specific transcriptional instructions? Here, we show that forcing a metabolic change in embryonic stem cells (ESCs) promotes a developmental identity that better approximates the inner cell mass (ICM) of the early mammalian blastocyst in cultures we refer to as enhanced metabolic ESCs (EMESCs). The creation of EMESCs depends on inhibition of glycolysis and stimulation of oxidative phosphorylation (OXPHOS), that in turns activates NAD+-dependent deacetylases of the Sirtuin family, resulting in the deacetylation of histones and key transcription factors to focus enhancer activity while reducing transcriptional noise, that result in a robust enhanced ESC phenotype. This exploitation of a NAD+/NADH coenzyme coupled to OXPHOS as a means of programming lineage specific transcription suggests new paradigms for how cells respond to alterations in their environment, and implies cellular rejuvenation exploits enzymatic activities to for simultaneous activation of a discrete enhancer set alongside silencing genome-wide transcriptional noise.

2025-04-01 | GSE252342 | GEO

Altering metabolism to program cell identity via NAD+ dependent deacetylation

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

2025-04-01 | GSE173543 | GEO

Altering metabolism programs cell identity via NAD+- dependent deacetylation

Project description:Cells change their metabolic profiles in response to underlying gene regulatory networks, but how can alterations in metabolism encode specific transcriptional instructions? Here, we show that forcing a metabolic change in embryonic stem cells (ESCs) promotes a developmental identity that better approximates the inner cell mass (ICM) of the early mammalian blastocyst in cultures. This shift in cellular identity depends on inhibition of glycolysis and stimulation of oxidative phosphorylation (OXPHOS) triggered by replacement of D-glucose by D-galactose in ESC media. Enhanced OXPHOS in turn activates NAD+-dependent deacetylases of the sirtuin family, resulting in deacetylation of histones and key transcription factors to focus enhancer activity while reducing transcriptional noise, that result in a robustly enhanced ESC phenotype. This exploitation of a NAD+/NADH coenzyme coupled to OXPHOS as a means of programming lineage-specific transcription suggests new paradigms for how cells respond to alterations in their environment, and implies cellular rejuvenation exploits enzymatic activities for simultaneous activation of a discrete enhancer set alongside silencing genome-wide transcriptional noise.

| S-SCDT-10_1038-S44318-025-00417-0 | biostudies-other

Elevated NAD+ drives Sir2A-mediated GCβ deacetylation and localization for Plasmodium ookinete gliding and mosquito infection

Project description:cGMP signal-activated ookinete gliding is essential for mosquito midgut infection of Plasmodium in malaria transmission. During ookinete development, cGMP synthesizer GCβ polarizes to a unique localization “ookinete extrados site” (OES) until ookinete maturation and activates cGMP signaling for initiating parasite motility. However, the mechanism underlying GCβ translocation from cytosol to OES remains elusive. Here, we used protein proximity labeling to search the GCβ-interacting proteins in ookinetes of the rodent malaria parasite P. yoelii, and found the top hit Sir2A, a NAD+-dependent sirtuin family deacetylase. Sir2A interacts with GCβ throughout ookinete development. In mature ookinetes, Sir2A co-localizes with GCβ at OES in a mutually dependent manner. Parasites lacking Sir2A lose GCβ localization at OES, ookinete gliding, and mosquito infection, phenocopying GCβ deficiency. GCβ is acetylated at gametocytes but is deacetylated by Sir2A for OES localization at mature ookinetes. We further demonstrated that the level of NAD+, an essential co-substrate for sirtuin, increases during the ookinete development. The NAD+ at its maximal level until ookinete maturation promotes Sir2A-catalyzed GCβ deacetylation, ensuring GCβ localization at OES. This study highlights the spatiotemporal coordination of cytosolic NAD+ level and NAD+-dependent Sir2A in regulating GCβ deacetylation and dynamic localization for Plasmodium ookinete gliding.

2024-09-26 | PXD056305 |

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