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Transglutaminase 2 regulates terminal erythroid differentiation via cross-linking activity

ABSTRACT: Transglutaminase 2 regulates terminal erythroid differentiation via cross-linking activity

PROVIDER: PRJNA955100 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24152534_1.fastq.gz	Fastqsanger.gz
	SRR24152534_2.fastq.gz	Fastqsanger.gz
	SRR24152535_1.fastq.gz	Fastqsanger.gz
	SRR24152535_2.fastq.gz	Fastqsanger.gz
	SRR24152536_1.fastq.gz	Fastqsanger.gz

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Transglutaminase 2 regulates terminal erythroid differentiation via cross-linking activity

Project description:To gain the whole picture of terminal erythroid differentiation, bone marrow erythroblasts of different maturation stages including proerythroblasts (Pro),basophilic erythroblasts (Baso), polychromatic erythroblasts (Poly) and orthochromatic erythroblasts (Ortho) were isolated and sorted.Transcriptomic analysis of these four stages of cells was performed.

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Project description:Terminal differentiation of mammalian erythroid progenitors involves 4-5 cell divisions and induction of many erythroid important genes, followed by chromatin and nuclear condensation and enucleation. The protein levels of c-myc (Myc) are reduced dramatically during late stage erythroid maturation, coinciding with cell cycle arrest in G1-phase and enucleation, suggesting possible roles for c-myc in either or both of these processes. Here we demonstrate that ectopic Myc expression affects terminal erythroid maturation in a dose-dependent manner. Expression of Myc at physiological levels did not affect erythroid differentiation or cell cycle shutdown, but specifically blocked erythroid nuclear condensation and enucleation. Myc prevented deacetylation of several lysine residues in histones H3 and H4 that are normally deacetylated during erythroid maturation. When over-expressed at levels higher than the physiological range, Myc blocked erythroid differentiation and the cells continued to proliferate in cytokine-free, serum-containing culture medium with an early erythroblast morphology. These studies reveal an important dose-dependent function of Myc in regulating terminal maturation in mammalian erythroid cells. Our findings further support the emerging notion that Myc regulates chromatin structure by regulating global histone acetylation states. Five groups with three biological replicates in each.

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