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A lineage commitment checkpoint in early ILC development [single cell RNA-seq]

ABSTRACT: A lineage commitment checkpoint in early ILC development [single cell RNA-seq]

PROVIDER: PRJNA453959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7073406.fastq.gz	Fastqsanger.gz
	SRR7073407.fastq.gz	Fastqsanger.gz
	SRR7073408.fastq.gz	Fastqsanger.gz

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A lineage commitment checkpoint in early ILC development

Project description:A lineage commitment checkpoint in early ILC development

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A lineage commitment checkpoint in early ILC development [bulk RNA-seq]

Project description:Understanding how cellular function is imprinted during development requires the identification of factors controlling lineage specification and commitment, and the intermediate progenitors in which they act. Using population level and single cell approaches, we examine transcriptional and functional heterogeneity within early innate lymphoid cells (ILC) progenitors. We identify a developmental bifurcation toward dendritic cell fate that reveals the uncommitted state of early specified ILC progenitors. We subsequently characterize an ILC-commitment checkpoint controlled by the transcription factor TCF-1. The present study reveals unexpected heterogeneity within early innate progenitor populations, and characterizes lineage infidelity that accompanies early ILC specification prior to commitment.

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A lineage commitment checkpoint in early ILC development [bulk RNA-seq]

Project description:A lineage commitment checkpoint in early ILC development [bulk RNA-seq]

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Zfp260 choreographs the early stage lineage commitment of skeletal stem cells

Project description:Zfp260 choreographs the early stage lineage commitment of skeletal stem cells

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A lineage commitment checkpoint in early ILC development

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

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A SIRT7-dependent acetylation switch regulates early B-cell differentiation and lineage commitment through PAX5

Project description:B lymphopoiesis is a key developmental event orchestrated by a complex combinatorial action of lineage-specific transcription factors. In early B cell progenitors, lineage commitment is directly mediated by the master regulator PAX5, whose deficiency is commonly associated with B cell Acute Lymphoblastic Leukemia (B-ALL). Despite its essential role in mammalian immunity, the regulatory mechanisms that control PAX5 function remain largely unknown. Here we show that NAD+-dependent enzyme SIRT7 coordinates B cell development progression through PAX5. We have identified a SIRT7-dependent regulatory switch based on dynamic deacetylation of a single PAX5 residue, which controls its activity and thereby B cell fate. While a PAX5K198 acetylated mimic is incapable of inducing both B cell development and identity due to reduced protein stability and impaired binding to chromatin, deacetylation of this residue boosts PAX5 activity, leading to massive gene repression and in vivo restoration of B cell commitment but not differentiation. These findings suggest an unexpected uncoupling of hematopoietic differentiation and lineage commitment. Further supporting the functional relevance of the SIRT7-PAX5 axis, the interplay between both factors is conserved in human B-ALL, where high SIRT7 expression is an independent good prognostic factor. Our findings unveil a crucial mechanism in the regulation of B cell production based on the control of PAX5 function and underscore the key role of Sirtuins in the regulation of the immune system.

2024-09-20 | PXD046457 | Pride

Early lineage commitment defines alveolar epithelial ontogeny in the lung

Project description:Early lineage commitment defines alveolar epithelial ontogeny in the lung

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ILC progenitor CEL-seq

Project description:Here we identify the c-kit+ CILP population which generates all ILC subsets including NK cells, and the CD25- ILC2-restricted Sca-1+ CILP. We mapped the transcriptional changes that occur in ILC progenitor commitment identifying new regulatory factors and provide a map for early ILC differentiation. Finally, we mapped the subsequent transcriptional changes that occur in c-kit+ CILP in absence of Id2 and Tcf7, key regulators downstream of Nfil3.

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Project description:During the step-wise specification and differentiation of tissue specific multipotent progenitor cells, lineage-specific transcriptional networks are either activated or repressed to orchestrate progenitor cell commitment. The gas exchange niche in the lung contains two major epithelial cell types, alveolar type 1 (AT1) and type 2 (AT2) cells, and the timing of lineage commitment of these cells is critical for correct formation of this niche and postnatal survival. To define the ontogeny of alveolar cell fate in the lung, we used lineage tracing studies combined with spatially specific mRNA transcript and protein expression combined with single cell RNA-seq analysis. These studies reveal that commitment to alveolar epithelial cell fate occurs far earlier than previously appreciated, concomitant with the proximal-distal specification of epithelial progenitors and branching morphogenesis. Using a novel dual lineage tracing system, we show that a small population of alveolar cells express markers of both AT1 and AT2 cells, whose fate is ultimately restricted to a single lineage. However, these bi-transcriptional cells generate only a minor portion of the mature alveolar epithelium. These data reveal a new paradigm of organ formation where early lineage commitment occurs during the nascent stages of development coincident with broad tissue patterning processes including axial patterning of the endoderm and branching morphogenesis.

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