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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells

ABSTRACT: IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells

PROVIDER: PRJNA730535 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14323557_1.fastq.gz	Fastqsanger.gz
	SRR14323557_2.fastq.gz	Fastqsanger.gz
	SRR14323558_1.fastq.gz	Fastqsanger.gz
	SRR14323558_2.fastq.gz	Fastqsanger.gz
	SRR14323559_1.fastq.gz	Fastqsanger.gz

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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [ChIP-seq]

Project description:IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [ChIP-seq]

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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [RNA-Seq]

Project description:IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [RNA-Seq]

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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [ChIP-seq]

Project description:Through a comparison between genes that are significant for growth and viability of AML cells by way of a CRISPR screen, with genes that are differentially expressed in leukemia stem cells, we identified importin 11 (IPO11) as a novel target in AML. In AML, knockdown of IPO11 decreased growth, reduced engraftment potential of stem cells and induced differentiation. Mechanistically, we identified the transcription factors BZW1 and BZW2 as novel cargoes of IPO11. We further show that BZW1/2 mediate a transcriptional signature that promotes stemness and survival of LSC.

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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells [RNA-Seq]

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Mitochondrial carrier homolog 2 (MTCH2) is necessary for AML survival

Project description:Through a CRISPR screen to identify mitochondrial genes necessary for the growth of AML cells, we identified the mitochondrial outer membrane protein MTCH2 (Mitochondrial Carrier Homolog 2). In AML, knockdown of MTCH2 decreased growth, reduced engraftment potential of stem cells and induced differentiation. Inhibiting MTCH2 altered in AML cells increased nuclear pyruvate and pyruvate dehydrogenase that induced histone acetylation and subsequently promoted the differentiation of AML cells. Thus, we have defined a new mechanism by which mitochondria and metabolism regulate AML stem cells and gene expression.

2020-03-25 | GSE147508 | GEO

IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells.

Project description:AML cells are arranged in a hierarchy with stem/progenitor cells giving rise to more differentiated bulk cells. Despite the importance of stem/progenitors in the pathogenesis of AML, the determinants of the AML stem/progenitor state are not fully understood. Through a comparison of genes that are significant for growth and viability of AML cells by way of a CRISPR screen, with genes that are differentially expressed in leukemia stem cells (LSC), we identified importin 11 (IPO11) as a novel target in AML. Importin 11 (IPO11) is a member of the importin β family of proteins that mediate transport of proteins across the nuclear membrane. In AML, knockdown of IPO11 decreased growth, reduced engraftment potential of LSC, and induced differentiation. Mechanistically, we identified the transcription factors BZW1 and BZW2 as novel cargo of IPO11. We further show that BZW1/2 mediate a transcriptional signature that promotes stemness and survival of LSC. Thus, we demonstrate for the first time how specific cytoplasmic-nuclear regulation supports stem-like transcriptional signature in relapsed AML.

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AKIRIN2 controls the nuclear import of proteasomes in vertebrates

Project description:Protein expression and turnover are controlled through a complex interplay of transcriptional, post-transcriptional and post-translational mechanisms to enable spatial and temporal regulation of cellular processes. To systematically elucidate such gene regulatory networks, we developed a CRISPR screening assay based on time-controlled Cas9 mutagenesis, intracellular immunostaining and fluorescence-activated cell sorting that enables the identification of regulatory factors independent of their effects on cellular fitness. We pioneered this approach by systematically probing the regulation of the transcription factor MYC, a master regulator of cell growth. Our screens uncover a highly conserved protein, AKIRIN2, that is essentially required for nuclear protein degradation. We found that AKIRIN2 forms homodimers that directly bind to fully assembled 20S proteasomes to mediate their nuclear import. During mitosis, proteasomes are excluded from condensing chromatin and re-imported into newly formed daughter nuclei in a highly dynamic, AKIRIN2-dependent process. Cells undergoing mitosis in the absence of AKIRIN2 become devoid of nuclear proteasomes, rapidly causing accumulation of MYC and other nuclear proteins. Collectively, our study reveals a dedicated pathway controlling the nuclear import of proteasomes in vertebrates and establishes a scalable approach to decipher regulators in essential cellular processes.

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AKIRIN2 controls the nuclear import of proteasomes in vertebrates

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Project description:Nuclear pores are essential pathways for nuclear-cytoplasmic transport of molecules. Whether and how cells change nuclear pores to alter nuclear transport and cellular function is unknown. Here, we show that heart muscle cells (cardiomyocytes) undergo a 63% decrease in nuclear pore numbers during differentiation, which alters their response to extracellular signals. This maturation-associated decline in nuclear pore numbers per nucleus is associated with lower nuclear levels and import of Mitogen-activated Protein Kinase (MAPK) signaling proteins. Experimental reduction of nuclear pore numbers decreased nuclear import of MAPK signaling proteins. In a mouse model of high blood pressure, reduction of cardiomyocyte nuclear pore numbers reduced adverse heart remodeling and gene regulation, which reduced progression to lethal heart failure. The observed decrease in nuclear pore numbers in cardiomyocyte differentiation and resulting functional changes suggest a paradigm by which terminally differentiated cells could permanently alter their handling of information flux across the nuclear envelope and, with that, their behavior.

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Project description:The goal of the project was to study the transcription rates and mRNA levels, genome-wide, in several mutants in Xrn1 defetive in nuclear import. We used Genomic Run-On (GRO) experiment in wild type and xrn1 mutant strains.

2022-09-30 | GSE158250 | GEO

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