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Human Hematopoietic Stem Cell Vulnerability to Ferroptosis [Ribosome profiling]

ABSTRACT: Human Hematopoietic Stem Cell Vulnerability to Ferroptosis [Ribosome profiling]

PROVIDER: PRJNA913269 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22767485.fastq.gz	Fastqsanger.gz
	SRR22767486.fastq.gz	Fastqsanger.gz
	SRR22767487.fastq.gz	Fastqsanger.gz
	SRR22767488.fastq.gz	Fastqsanger.gz
	SRR22767489.fastq.gz	Fastqsanger.gz

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Human Hematopoietic Stem Cell Vulnerability to Ferroptosis

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Human Hematopoietic Stem Cell Vulnerability to Ferroptosis [Ribosome profiling]

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Human hematopoietic stem cell vulnerability to ferroptosis.

Project description:Hematopoietic stem cells (HSCs) have a number of unique physiologic adaptations that enable lifelong maintenance of blood cell production, including a highly regulated rate of protein synthesis. Yet, the precise vulnerabilities that arise from such adaptations have not been fully characterized. Here, inspired by a bone marrow failure disorder due to the loss of the histone deubiquitinase MYSM1, characterized by selectively disadvantaged HSCs, we show how reduced protein synthesis in HSCs results in increased ferroptosis. HSC maintenance can be fully rescued by blocking ferroptosis, despite no alteration in protein synthesis rates. Importantly, this selective vulnerability to ferroptosis not only underlies HSC loss in MYSM1 deficiency but also characterizes a broader liability of human HSCs. Increasing protein synthesis rates via MYSM1 overexpression makes HSCs less susceptible to ferroptosis, more broadly illustrating the selective vulnerabilities that arise in somatic stem cell populations as a result of physiologic adaptations.

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Runx1 deficiency decreases ribosome biogenesis and confers stress resistance to hematopoietic stem and progenitor cells

Project description:The transcription factor RUNX1 is frequently mutated in myelodysplastic syndrome and leukemia. RUNX1 mutations can be early events, creating pre-leukemic stem cells that expand in the bone marrow. Here we show that, counter-intuitively, Runx1 deficient hematopoietic stem and progenitor cells (HSPCs) have a slow growth, low biosynthetic, small cell phenotype and markedly reduced ribosome biogenesis (Ribi). The reduced Ribi involves decreased levels of rRNA and many mRNAs encoding ribosome proteins. Runx1 appears to directly regulate Ribi; Runx1 is enriched on the promoters of genes encoding ribosome proteins, and binds the ribosomal DNA repeats. Runx1 deficient HSPCs have lower p53 levels, reduced apoptosis, an attenuated unfolded protein response, and accordingly are resistant to genotoxic and endoplasmic reticulum stress. The low biosynthetic activity and corresponding stress resistance provides a selective advantage to Runx1 deficient HSPCs, allowing them to expand in the bone marrow and outcompete normal HSPCs. Comparison of the phenotypic and molecular properties of normal (Runx1f/f, or WT) versus Runx1 deficient (Mut) hematopoietic stem cells.

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Human Hematopoietic Stem Cell Vulnerability to Ferroptosis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Plasticity of ether lipids promotes ferroptosis susceptibility and evasion

Project description:Ferroptosis, an iron-dependent, non-apoptotic cell death program, is involved in a variety of degenerative diseases and represents a targetable vulnerability in certain cancers. The ferroptosis-susceptible cell-state can either preexist in cells arising from certain lineages or be acquired during cell-state transitions. Precisely how ferroptosis susceptibility is dynamically regulated remains poorly understood. Using genome-wide CRISPR/Cas9 suppressor screens, we identify a key role for peroxisome–ether phospholipid genes in driving ferroptosis susceptibility and evasion in ovarian cancer.

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Hematopoietic stem cells (HSCs)

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Ribosome stalling during selenoprotein translation exposes a ferroptosis vulnerability.

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