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Loss of epigenetic regulation disrupts lineage commitment and promotes breast cancer (scRNA-Seq)

ABSTRACT: Loss of epigenetic regulation disrupts lineage commitment and promotes breast cancer (scRNA-Seq)

PROVIDER: PRJNA738939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14855024.fastq.gz	Fastqsanger.gz
	SRR14855025.fastq.gz	Fastqsanger.gz
	SRR14855026.fastq.gz	Fastqsanger.gz
	SRR14855027.fastq.gz	Fastqsanger.gz
	SRR14855028.fastq.gz	Fastqsanger.gz

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Loss of epigenetic regulation disrupts lineage commitment and promotes breast cancer

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Loss of epigenetic regulation disrupts lineage commitment and promotes breast cancer (scRNA-Seq)

Project description:Systematically investigating the scores of genes mutated in cancer to discern the real drivers from the inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we use CRISPR/Cas9-mediated somatic gene editing in a breast cancer mouse model to assess the transforming potential of 215 recurrent ‘long-tail’ breast cancer genes. Several core and accessory components of the COMPASS-like histone methylase complex, namely KMT2C, KDM6A and ASXL2 cooperated with PIK3CAH1047R mutation to accelerate mammary tumorigenesis in mice and to transform human breast epithelial cells. Mechanistically, mutations of these ‘EpiDrivers’ converged on enhancing the lineage conversion of basal cells to luminal cells prior to tumorigenesis, as well as an aberrant alveolar differentiation program in both luminal and basal cells. Overall, our work suggests that lactation mimicry is associated with the earliest steps of breast cancer.

2022-09-12 | GSE178423 | GEO

Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis

Project description:Khajuria RK, Munschauer M, Ulirsch JC, Fiorini C, Leif S. Ludwig LS, McFarland SK, Abdulhay NJ, Specht H, Keshishian H, Mani DR, Jovanovic M, Ellis SR, Fulco CP, Engreitz JM, Schütz S, Lian J, Gripp KW,Weinberg OK, Pinkus GS, Gehrke L, Regev A, Lander ES, Gazda HT, Lee WY, Panse VG, Carr SA, Sankaran VG. Cell 2018, 173, 90–103. https://doi.org/10.1016/j.cell.2018.02.036. Blood cell formation is classically thought to occur through a hierarchical differentiation process, although recent studies have shown that lineage commitment may occur earlier in hematopoietic stem and progenitor cells (HSPCs). The relevance to human blood diseases and the underlying regulation of these refined models remain poorly understood. By studying a genetic blood disorder, Diamond-Blackfan anemia (DBA), where the majority of mutations affect ribosomal proteins and the erythroid lineage is selectively perturbed, we are able to gain mechanistic insight into how lineage commitment is programmed normally and disrupted in disease. We show that in DBA, the pool of available ribosomes is limited, while ribosome composition remains constant. Surprisingly, this global reduction in ribosome levels more profoundly alters translation of a select subset of transcripts. We show how the reduced translation of select transcripts in HSPCs can impair erythroid lineage commitment, illuminating a regulatory role for ribosome levels in cellular differentiation.

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Project description:Lineage commitment and differentiation is driven by the concerted action of master transcriptional regulators at their target chromatin sites. Multiple efforts have characterized the key transcription factors (TFs) that determine the various hematopoietic lineages. However, the temporal interactions between individual TFs and their chromatin targets during differentiation and how these interactions dictate lineage commitment remains poorly understood. We performed dense, daily, temporal profiling of chromatin accessibility (DNase I-seq) and gene expression changes (total RNA-seq) along ex vivo human erythropoiesis to comprehensively define developmentally regulated DNase I hypersensitive sites (DHSs) and transcripts. We link both distal DHSs to their target gene promoters and individual TFs to their target DHSs, revealing that the regulatory landscape is organized in distinct sequential regulatory modules that regulate lineage restriction and maturation. Finally, direct comparison of transcriptional dynamics (bulk and single-cell) and lineage potential between erythropoiesis and megakaryopoiesis uncovers differential fate commitment dynamics between the two lineages as they exit the stem and progenitor stage. Collectively, these data provide novel insights into the global regulatory landscape during hematopoiesis.

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