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Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

ABSTRACT: Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

PROVIDER: PRJNA987998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25045908_1.fastq.gz	Fastqsanger.gz
	SRR25045908_2.fastq.gz	Fastqsanger.gz
	SRR25045909_1.fastq.gz	Fastqsanger.gz
	SRR25045909_2.fastq.gz	Fastqsanger.gz
	SRR25045910_1.fastq.gz	Fastqsanger.gz

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Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

Project description:To elucidate the mechanisms underlying the role of Atf4 deficiency in erythropoiesis, we performed 10X Genomics single-cell RNA sequencing on Lin-cKit+ cells from Atf4 hematopoietic cell-specific conditional knockout mice (KO) and Atf4 floxed mice (WT) at steady state (referred to KO_BM and WT_BM) and after secondary transplantation (referred to cKO_t and WT_t). Furthermore, we also sorted CMP cells from Atf4 hematopoietic cell-specific conditional knockout mice (KO) and ATF4 floxed mice (WT) for 10X Genomics scRNA-seq.

2024-03-15 | GSE235798 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

Project description:The role of ribosome biogenesis in erythroid development is supported by the recognition of erythroid defects in ribosomopathies in both Diamond-Blackfan anemia and 5q- syndrome. Whether ribosome biogenesis exerts a regulatory function on normal erythroid development is still unknown. In the present study, a detailed characterization of ribosome biogenesis dynamics during human and murine erythropoiesis shows that ribosome biogenesis is abruptly interrupted by the drop of rDNA transcription and the collapse of ribosomal protein neo-synthesis. Its premature arrest by RNA polI inhibitor, CX-5461 targets the proliferation of immature erythroblasts. We also show that p53 is activated spontaneously or in response to CX-5461 concomitantly to ribosome biogenesis arrest, and drives a transcriptional program in which genes involved in cell cycle arrest, negative regulation of apoptosis and DNA damage response were upregulated. RNA polI transcriptional stress results in nucleolar disruption and activation of ATR-CHK1-p53 pathway. Our results imply that the timing of ribosome biogenesis extinction and p53 activation are crucial for erythroid development. In ribosomopathies in which ribosome availability is altered by unbalanced production of ribosomal proteins, the threshold of ribosome biogenesis down-regulation could be prematurely reached and together with pathological p53 activation prevents a normal expansion of erythroid progenitors.

2020-09-14 | GSE137951 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

2020-09-14 | GSE157208 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

| PRJNA660448 | ENA

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

| PRJNA573943 | ENA

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

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Bmi1 promotes erythroid development through regulating ribosome biogenesis.

Project description:While Polycomb group protein Bmi1 is important for stem cell maintenance, its role in lineage commitment is largely unknown. We have identified Bmi1 as a novel regulator of erythroid development. Bmi1 is highly expressed in mouse erythroid progenitor cells and its deficiency impairs erythroid differentiation. BMI1 is also important for human erythroid development. Furthermore, we discovered that loss of Bmi1 in erythroid progenitor cells results in decreased transcription of multiple ribosomal protein genes and impaired ribosome biogenesis. Bmi1 deficiency stabilizes p53 protein, leading to upregulation of p21 expression and subsequent G0/G1 cell cycle arrest. Genetic inhibition of p53 activity rescues the erythroid defects seen in the Bmi1 null mice, demonstrating that a p53-dependent mechanism underlies the pathophysiology of the anemia. Mechanistically, Bmi1 is associated with multiple ribosomal protein genes and may positively regulate their expression in erythroid progenitor cells. Thus, Bmi1 promotes erythroid development, at least in part through regulating ribosome biogenesis. Ribosomopathies are human disorders of ribosome dysfunction, including Diamond-Blackfan anemia (DBA) and 5q- syndrome, in which genetic abnormalities cause impaired ribosome biogenesis, resulting in specific clinical phenotypes. We observed that BMI1 expression in human hematopoietic stem and progenitor cells from patients with DBA is correlated with the expression of some ribosomal protein genes, suggesting that BMI1 deficiency may play a pathological role in DBA and other ribosomopathies.

| S-EPMC4380436 | biostudies-literature

Nucleolar Protein Nop2 Promotes Neural Differentiation by Regulating Ribosome Biogenesis-related Processes

Project description:Nucleolar Protein Nop2 Promotes Neural Differentiation by Regulating Ribosome Biogenesis-related Processes

| PRJNA1321709 | ENA

Nucleolar Protein Nop2 Promotes Neural Differentiation by Regulating Ribosome Biogenesis-related Processes

Project description:The NOP2 nucleolar protein (NOP2) serves pivotal functions in ribosome biogenesis, cell cycle regulation and embryonic development, yet its spatiotemporal dynamics and mechanistic contributions to neural development remain elusive. Through CRISPR/Cas9-mediated knockout modeling in zebrafish, we demonstrated that NOP2 nucleolar protein homolog (yeast) (nop2) deficiency induced embryonic lethality within 3-5 days post-fertilization (dpf), accompanied by pathognomonic microcephaly and cerebral edema. Mechanistic analysis suggested that nop2 ablation triggered differentiation impairment in neural progenitors, which accumulated extensively in brain tissue and led to impaired generation of neurons and glial cells. In addition, nop2 deficiency activated p53-dependent apoptosis in neural cells. Biochemical characterization revealed compromised pre-ribosomal particle processing in mutants, establishing defective ribosome biogenesis as the primary molecular lesion. Ribosome profiling (Ribo-seq) uncovered aberrant regulation of nervous system processes and activation of p53-mediated apoptosis in neural cells. Genetic epistasis experiments demonstrated that tp53 mutation partially rescued neurogenic defects and reduced cerebral edema, but failed to rescue microcephaly. These findings provide evidence supporting the role of Nop2 as a significant regulator in neural development. Our results demonstrate that Nop2 promotes neural differentiation by regulating ribosome biogenesis-related processes, thereby extending our previous research on rRNA metabolism-related genes in neurodevelopment. Moreover, our study provides critical insights into developing early interventions against neurodevelopmental disorders associated with ribosomopathies.

2026-03-01 | GSE307442 | GEO

NOC4L coordinates neuronal and pharyngeal arch development by regulating ribosome biogenesis-related processes

Project description:NOC4L coordinates neuronal and pharyngeal arch development by regulating ribosome biogenesis-related processes

| PRJNA1238785 | ENA