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Transcriptionally regulated energy metabolism drives early erythropoiesis (ChIP-Seq)

ABSTRACT: Transcriptionally regulated energy metabolism drives early erythropoiesis (ChIP-Seq)

PROVIDER: PRJNA562553 | ENA |

REPOSITORIES: ENA

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Transcriptionally regulated energy metabolism drives early erythropoiesis

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis

| PRJNA562552 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (RRBS)

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis (RRBS)

| PRJNA686370 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (RNA-Seq)

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis (RNA-Seq)

| PRJNA562554 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (tif1g RNA-seq)

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis (tif1g RNA-seq)

| PRJNA686149 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (mon RNA-seq)

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis (mon RNA-seq)

| PRJNA686152 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (ChIP-Seq)

Project description:Transcription and metabolism both influence cell function but dedicated transcriptional control of metabolic pathways regulating cell fate has rarely been defined. Zebrafish moonshine mutant embryos defective for the transcription elongation factor tif1γ do not make red blood cells. Here, through a chemical suppressor screen we discovered that inhibition of the pyrimidine biosynthesis enzyme DHODH rescues erythroid differentiation in moonshine mutant embryos, which depends on the functional link of DHODH to mitochondrial coenzyme Q activity. In-vivo metabolomics analysis reveals that tif1γ loss results in mitochondrial respiration defects that are associated with reduced expression of genes that encode coenzyme Q synthesis enzymes and are directly bound and controlled by TIF1γ. Treatment of moonshine embryos with a coenzyme Q analogue rescues their bloodless defect. These results demonstrate energy metabolism is a key output of a lineage transcription factor that drives cell fate decisions in the early blood lineage.

2021-06-09 | GSE136452 | GEO

Transcriptionally regulated energy metabolism drives early erythropoiesis (RNA-Seq)

2021-06-09 | GSE136453 | GEO

Transcriptionally regulated energy metabolism drives early erythropoiesis (RRBS)

Project description:Transcription and metabolism both influence cell function yet dedicated transcriptional control of metabolic pathways that regulate cell fate has rarely been defined. Through a chemical suppressor screen, we discovered that inhibition of the pyrimidine biosynthesis enzyme DHODH rescues erythroid differentiation in bloodless moonshine mutant embryos defective for the transcription elongation factor tif1γ. This rescue depends on the functional link of DHODH to mitochondrial respiration. TIF1γ directly controls coenzyme Q synthesis gene expression. Upon tif1γ loss, coenzyme Q levels are reduced, and a high succinate/α-ketoglutarate ratio leads to increased histone methylation. A coenzyme Q analogue rescues moonshine’s bloodless phenotype. These results demonstrate mitochondrial metabolism is a key output of a lineage transcription factor that drives cell fate decisions in the early blood lineage.

2021-06-09 | GSE163483 | GEO

Transcriptionally regulated energy metabolism drives early erythropoiesis (mon RNA-seq)

Project description:Transcription and metabolism both influence cell function yet dedicated transcriptional control of metabolic pathways that regulate cell fate has rarely been defined. Through a chemical suppressor screen, we discovered that inhibition of the pyrimidine biosynthesis enzyme DHODH rescues erythroid differentiation in bloodless moonshine mutant embryos defective for the transcription elongation factor tif1γ. This rescue depends on the functional link of DHODH to mitochondrial respiration. Low α-ketoglutarate levels caused by tif1γ loss lead to histone hypermethylation. TIFγ directly controls coenzyme Q synthesis gene expression and coenzyme Q levels are reduced in moonshine mutants. A coenzyme Q analogue rescues moonshine’s bloodless phenotype. These results demonstrate mitochondrial metabolism is a key output of a lineage transcription factor that drives cell fate decisions in the early blood lineage.

2021-06-09 | GSE163454 | GEO

Transcriptionally regulated energy metabolism drives early erythropoiesis (tif1g RNA-seq)

Project description:Transcription and metabolism both influence cell function yet dedicated transcriptional control of metabolic pathways that regulate cell fate has rarely been defined. Through a chemical suppressor screen, we discovered that inhibition of the pyrimidine biosynthesis enzyme DHODH rescues erythroid differentiation in bloodless moonshine mutant embryos defective for the transcription elongation factor tif1γ. This rescue depends on the functional link of DHODH to mitochondrial respiration. Low α-ketoglutarate levels caused by tif1γ loss lead to histone hypermethylation. TIFγ directly controls coenzyme Q synthesis gene expression and coenzyme Q levels are reduced in moonshine mutants. A coenzyme Q analogue rescues moonshine’s bloodless phenotype. These results demonstrate mitochondrial metabolism is a key output of a lineage transcription factor that drives cell fate decisions in the early blood lineage.

2021-06-09 | GSE163453 | GEO

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