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

ABSTRACT: 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.

ORGANISM(S): Danio rerio

PROVIDER: GSE163454 | GEO | 2021/06/09

REPOSITORIES: GEO

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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

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 (RNA-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 | GSE136453 | GEO

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

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An aging-like phenotype occurs in Tif1γ-/- hematopoietic stem cells

Project description:To determine whether an accelerated aging-like phenotype occurs in hematopoiesis of young Tif1γ-/- mice (4 months old), we purified 200,000 hematopoietic stem cells (LSK: Lineage negative, Sca1+, c-Kit+) from Tif1γ-/- mice and performed high-throughput mRNA sequencing (RNA-seq). We compared this transcriptome to physiological aging by creating two other RNAseq libraries from young (4 months old) and old (20 months old) wild type mice. RNAseq study on young Tif1γ-/- mice (4 months old), young wild type mice (4 months old) and old wild type mice (20 months old).

2014-06-16 | E-GEOD-57396 | biostudies-arrayexpress

An aging-like phenotype occurs in Tif1γ-/- hematopoietic stem cells

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The Stat3-Fam3a axis promotes muscle stem cell myogenic lineage progression by inducing mitochondrial respiration

Project description:Metabolic reprogramming is an active regulator of stem cell fate choices, and successful stem cell differentiation in different compartments requires the induction of oxidative phosphorylation. However, the mechanisms that promote mitochondrial respiration during stem cell differentiation are poorly understood. Here we demonstrate that Stat3 promotes muscle stem cell myogenic lineage progression by stimulating mitochondrial respiration. We identify Fam3a, a cytokine-like protein, as a major Stat3 downstream effector in muscle stem cells. We demonstrate that Fam3a is required for muscle stem cell commitment and skeletal muscle development. We show that myogenic cells secrete Fam3a, and exposure of Stat3-ablated muscle stem cells to recombinant Fam3a in vitro and in vivo rescues their defects in mitochondrial respiration and myogenic commitment. Together, these findings indicate that Fam3a is a Stat3-regulated secreted factor that promotes muscle stem cell oxidative metabolism and differentiation, and suggests that Fam3a is a potential tool to modulate cell fate choices.

2019-03-19 | GSE128527 | GEO

Gene expression in the mitochondrial syndrome of coenzyme Q deficiency

Project description:Coenzyme Q10 deficiency syndrome includes a clinically heterogeneous group of mitochondrial diseases characterized by low content of CoQ10 in tissues. The only currently available treatment is supplementation with CoQ10, which improves the clinical phenotype in some patients but does not reverse established damage. Incubation with CoQ10 restored respiration and apoptotic pathways but did not affect lipid metabolism, cell growth, and undifferentiated phenotype presented by CoQ10 deficient cells. We conclude that the mitochondrial dysfunction caused byCoQ10 deficiency induces a stable survival adaptation of somatic cells from patients, thus explaining their incomplete recovery after treatment. We compared the gene expresion of human dermal fibroblast from healthy people (group 1) with fibroblast from diferent patient diagnosed with the human syndrome of coenzyme Q10 deficiency, which were treated (group 3) or not (group 2) with coenzyme Q10 to recovery ATP levels.

2013-04-05 | E-GEOD-33940 | biostudies-arrayexpress

Effect of TIF1γ gene deletion on hematopoietic stem cells

Project description:Analysis of KLS cells purified from bone marrow of mice conditionally inactivated for TIF1γ gene. TIF1γ deletion results in multiple defects in adult hematopoiesis. Results provide insight into the role of TIF1γ in hematopoietic stem cells functions. We used microarrays to characterize the molecular mechanisms underlying the biological properties of KLS cells lacking TIF1γ KLS (lin-,c-kit+, Sca+) cells were purified by cell sorting

2012-06-24 | E-GEOD-22280 | biostudies-arrayexpress

Effect of TIF1γ gene deletion on hematopoietic stem cells

2012-06-25 | GSE22280 | GEO

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