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Fetal specific human B-cell developmental programs

ABSTRACT: Fetal specific human B-cell developmental programs

PROVIDER: PRJNA507185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8247790_1.fastq.gz	Fastqsanger.gz
	SRR8247790_2.fastq.gz	Fastqsanger.gz
	SRR8247800_1.fastq.gz	Fastqsanger.gz
	SRR8247800_2.fastq.gz	Fastqsanger.gz
	SRR8247850_1.fastq.gz	Fastqsanger.gz

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A novel human fetal liver-derived model reveals that MLL-AF4 drives fetal gene expression programs in infant ALL [ChIP-seq]

Project description:Although 90% of children with acute lymphoblastic leukemia (ALL) are now cured, the prognosis of infant-ALL (diagnosis within the first year of life) remains dismal. Infant-ALL is usually caused by a single genetic hit that arises in utero: rearrangement of the MLL/KMT2A gene (MLL-r). This is sufficient to give rise to a uniquely aggressive and treatment-refractory leukemia compared to older children with the same MLL-r. The reasons for disparate outcomes in patients of different ages with identical molecular drivers are unknown. This paper addresses the hypothesis that fetal-specific gene expression programs co-operate with MLL-AF4 to initiate and maintain infant-ALL. Using direct comparison of fetal and adult HSC and progenitor transcriptomes we identify fetal-specific gene expression programs in primary human cells. We show that MLL-AF4-driven infant-ALL, but not MLL-AF4 childhood-ALL, displays expression of fetal-specific genes. In a direct test of this observation, we find that CRISPR-Cas9 gene editing of primary human fetal liver cells (to produce a t(4;11)/MLL-AF4 translocation) replicates the clinical features of infant-ALL and drives infant-ALL-specific and fetal-specific gene expression programs. These data strongly support the hypothesis that fetal-specific gene expression programs co-operate with MLL-AF4 to initiate and maintain the distinct biology of infant ALL.

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Single-cell multiomics of human fetal hematopoiesis defines a developmental specific population and a fetal signature

Project description:Knowledge of human fetal blood development and how it differs from adult is highly relevant to our understanding of congenital blood and immune disorders and childhood leukemia, of which the latter can originate in utero. Blood formation occurs in waves that overlap in time and space adding to heterogeneity, which necessitates single-cell approaches. Here, a combined single cell immunophenotypic and transcriptional map of first trimester primitive blood development is presented. Using CITE-seq (Cellular-Indexing-of-Transcriptomes-and-Epitopes-by-Sequencing) the molecular profile of established immunophenotypic gated progenitors was analyzed in the fetal liver (FL). Classical markers for hematopoietic stem cells (HSCs) such as CD90 and CD49F were largely preserved, whereas CD135 (FLT3) and CD123 (IL3R) had a ubiquitous expression pattern capturing heterogenous populations. Direct molecular comparison with an adult bone marrow (BM) dataset revealed that the HSC state was less frequent in FL, whereas cells with lympho-myeloid signature were more abundant. An erythro-myeloid primed multipotent progenitor cluster was identified, potentially representing a transient, fetal-specific population. Furthermore, differentially expressed genes between fetal and adult counterparts were specifically analyzed, and a fetal core signature identified. The core gene set could separate subgroups of Acute Lymphoblastic Leukemia (ALL) by age, suggesting that a fetal program may be partially retained in specific sub-groups of pediatric leukemia. Our detailed single-cell map presented herein emphasizes molecular and immunophenotypic differences between fetal and adult blood cells, of significance for future studies of pediatric leukemia and blood development in general.

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