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RNA-seq of granulocytes derived from control and AK2 depleted human HSPCs

ABSTRACT: RNA-seq of granulocytes derived from control and AK2 depleted human HSPCs

PROVIDER: PRJNA743237 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15021753_1.fastq.gz	Fastqsanger.gz
	SRR15021753_2.fastq.gz	Fastqsanger.gz
	SRR15021754_1.fastq.gz	Fastqsanger.gz
	SRR15021754_2.fastq.gz	Fastqsanger.gz
	SRR15021755_1.fastq.gz	Fastqsanger.gz

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RNA-seq of granulocytes derived from control and AK2 depleted human HSPCs

Project description:Reticular Dysgenesis (RD) is a rare but devastating form of severe combined immunodeficiency, characterized by a maturation arrest of the myeloid and lymphoid lineages paired with sensorineural hearing loss. RD is caused by biallelic loss-of-function mutations in the mitochondrial enzyme adenylate kinase 2 (AK2). To study the effect of AK2 depletion on HSPC differentiation, we developed a biallelic AK2 CRISPR knock-out model using human HSPCs. AK2 depleted HSPCs display severe proliferation and myeloid differentiation defects, recapitulating RD patient phenotype.

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Project description:Reticular dysgenesis (RD) is a human Severe Combined Immunodeficiency mainly characterized by a profound neutropenia and lymphopenia. This pathology is due to mutations in the adenylate kinase 2 (AK2) gene, resulting in the loss of AK2 protein expression. AK2 is a mitochondrial protein, which regulates the homeostasis of cellular adenine nucleotides by converting ADP into ATP and AMP. Using a RNA interference strategy, we dissected the role of AK2 during the commitment of hematopoietic progenitors towards the lymphoid or myeloid lineage. Our results demonstrated that AK2 knock-down progenitors have reduced proliferative and survival capacity and differentiation toward the lymphoid or granulocytic lineage is abrogated. In this report, we also highlighted that AK2 signaling pathway is essential to control energy production and to maintain the integrity of all mitochondrial functions. This steady state may be disturbed in RD patients leading to a blockade of the differentiation process.

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Project description:Recent studies have linked bioenergetic regulation to cellular differentiation. However, the contribution of metabolic communication among subcellular components to the fate of progenitor cells remains unclear. Adenylate kinase 2 (AK2) is an adenylate phosphotransferase localized in the mitochondrial intermembrane space. Although AK2 mutations in human can cause a severe combined immunodeficiency with neutropenia, named reticular dysgenesis (RD), underlying mechanisms have not yet been elucidated. To address these questions, we established induced pluripotent stem cells (iPSCs) from two RD patients. Metabolic flux analysis revealed that AK2 mediates the distribution of glycolytic metabolites into the tricarbon acid cycle in mitochondria. Hematopoietic differentiation from RD-iPSCs was profoundly impaired. Intriguingly, RD-iPSC-derived hematopoietic progenitors exhibited an immature mitochondrial morphology, discordant ATP distribution among the mitochondria and nucleus, and alteration of global transcriptional profiles. These results highlight the importance of stage-specific intracellular energy communication for controlling the fate of multipotential progenitors.

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Project description:AK2 is n-terminally processed by methionine aminopeptidases, N-terminal acetylation and DDP8/9 to become an active protein which is then sorted in the mitochondrial intermembrane space. We used peptide pull-downs of free and acetylated N-terminal peptides of AK2 from the different processing steps to identify binding partners by MS. We identified the inhibitor of apoptosis E3 ligase proteins (IAPs; BIRC2, 3, 6 and XIAP) as new binding partners for processed AK2 and show that they are responsible for AK2 degradation in the cytosol.

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Project description:To investigate the changes in gene expression during the process of differentiation into neutrophils and to evaluate the effect of Ak2 hetero-knockout in the process, microarray analysis was performed. HL-60 Ak2 hetero-knockout clone #47 cells were cultured with all-trans retinoic acid (ATRA) for 4 days. The cells were collected at four different time points and total RNA was prepared for use as a sample for microarray analysis.

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Histone chromatin modifications in control and Med12-deficient mouse HSPCs

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