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A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification

ABSTRACT: A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification

PROVIDER: PRJNA1005234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25634635_1.fastq.gz	Fastqsanger.gz
	SRR25634635_2.fastq.gz	Fastqsanger.gz
	SRR25634636_1.fastq.gz	Fastqsanger.gz
	SRR25634636_2.fastq.gz	Fastqsanger.gz
	SRR27586136_1.fastq.gz	Fastqsanger.gz

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A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification

Project description:The Drosophila tracheal system emerges as a favorable model for investigating the program of tubular morphogenesis. It is established in the embryo by post-mitotic cells, which also undergoes remodeling by modulating stem cells. Here we provide an analysis of a comprehensive cell atlas of Drosophila trachea using single-cell RNA-sequencing (scRNA-seq) and reveal cellular diversity and transcriptional profiles of tracheoblasts in Drosophila airway, which encompasses 9 major subtypes. Further evidences reveal transcription factors that are able to switch cell fate. The transcription factors, Peb, Bs, Kni, Sal and Cut are influenced by Notch signaling and determine cell identity. Moreover, Notch signaling that is responsible for the differentiation of tracheoblasts responds to protein glycosylation that is induced upon high sugar diet. Therefore, our study provides a transcriptomic atlas of tracheal development and regeneration, and suggests a glycosylation-responsive Notch signaling in cell fate determination.

2024-02-18 | GSE240777 | GEO

GATA3 induces human T cell commitment following Notch-induced T-lineage specification (expression)

Project description:Here, we show that GATA3 induces T-lineage commitment following Notch-induced T-lineage specification through direct regulation of at least 3 distinct processes: repression of NK-cell fate, activation of T-lineage genes to promote further differentiation, and down modulation of Notch signalling activity. Gene expression was measured in RPMI8402 cells after transduction with control, shGATA3 or shTCF1 and culture for 48h. Cells were collected 48h after transduction and sorted for EGFP+. This was performed for 2 replicates.

2016-04-06 | E-GEOD-76348 | biostudies-arrayexpress

GATA3 induces human T cell commitment following Notch-induced T-lineage specification (expression)

2016-04-06 | GSE76348 | GEO

Single cell atlas of the aging mouse trachea

Project description:Single cell atlas of the aging mouse trachea

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GATA3 restrains Notch signaling activity and represses NK cell development to induce human T cell commitment following Notch-induced T-lineage specification (ChIP-Seq)

Project description:The stepwise conversion of multipotent precursors into committed T-cell progenitors depends on several transcriptional regulators, but the interplay between these factors is still obscure. This is particularly true in human since the core early Notch signalling pathway also supports NK cell development and requires tight regulation for efficient T-lineage commitment and differentiation. Here, we show that GATA3, in contrast to TCF1, induces T-lineage commitment following NOTCH1-induced T-lineage specification through direct regulation of at least 3 distinct processes: repression of NK-cell fate, activation of T-lineage genes to promote further differentiation, and downmodulation of Notch signalling activity. GATA3-mediated repression of the NOTCH1 target gene DTX1 hereby is essential to induce T-lineage commitment at the expense of NK cell differentiation. Thus, human T-lineage commitment is dependent on the precise collaboration of several transcriptional regulators that integrate through both positive and negative regulatory loops. ChIP-sequencing data was generated for GATA3 in human thymocytes

2016-04-06 | E-GEOD-71751 | biostudies-arrayexpress

GATA3 restrains Notch signaling activity and represses NK cell development to induce human T cell commitment following Notch-induced T-lineage specification (expression)

Project description:The stepwise conversion of multipotent precursors into committed T-cell progenitors depends on several transcriptional regulators, but the interplay between these factors is still obscure. This is particularly true in human since the core early Notch signalling pathway also supports NK cell development and requires tight regulation for efficient T-lineage commitment and differentiation. Here, we show that GATA3, in contrast to TCF1, induces T-lineage commitment following NOTCH1-induced T-lineage specification through direct regulation of at least 3 distinct processes: repression of NK-cell fate, activation of T-lineage genes to promote further differentiation, and downmodulation of Notch signalling activity. GATA3-mediated repression of the NOTCH1 target gene DTX1 hereby is essential to induce T-lineage commitment at the expense of NK cell differentiation. Thus, human T-lineage commitment is dependent on the precise collaboration of several transcriptional regulators that integrate through both positive and negative regulatory loops. Gene expression was profiled in CT CD34+ cells after transduction with control or GATA3 and coculture on OP9-DL1 for 48h. Cells were collected 48h after coculture and sorted for CD45+EGFP+. 3 independent experiments were performed on 3 different thymus donors.

2016-04-06 | E-GEOD-71752 | biostudies-arrayexpress

T cell factor 1 is a gatekeeper for T-cell specification in response to Notch signaling

Project description:Although transcriptional programs associated with T-cell specification and commitment have been described, the functional hierarchy and the roles of key regulators in structuring/ orchestrating these programs remain unclear. Activation of Notch signaling in uncommitted precursors by the thymic stroma initiates the T-cell differentiation program. One regulator first induced in these precursors is the DNA binding protein Tcf-1, a T-cell specific mediator of Wnt signaling. Yet the specific contribution of Tcf-1 to early T-cell development and the signals inducing it in these cells remain unclear. Here we assign functional significance to Tcf-1 as a gatekeeper of T-cell fate. We show that Tcf-1 is directly activated by Notch signals. Tcf-1 is required at the earliest phase of Tcell determination for progression beyond the early thymic progenitor (ETP) stage. The global expression profile of Tcf-1 deficient progenitors indicates that basic processes of DNA metabolism are downregulated in its absence and the blocked T-cell progenitors become abortive and die by apoptosis. Our data thus add an important functional relationship to the roadmap of T-cell development. We used microarrays to detail the global programme of gene expression of mouse ETP thymocyte after Ikaros inactivation with dominant negative of Ik at different stage. 6 samples (mouse ETP thymocytes from wt, and Tcf1 inactivation) are analyzed Mouse Microarray Expression platforms, Affymetrix Mouse 430 2.0,

2011-12-06 | E-GEOD-33513 | biostudies-arrayexpress

GATA3 restrains Notch signaling activity and represses NK cell development to induce human T cell commitment following Notch-induced T-lineage specification (expression)

2016-04-06 | GSE71752 | GEO

Role of Notch signaling on hematopoietic stem cell differentiation

Project description:Although Notch signaling has been clearly implicated in lymphoid differentiation, its role in myeloid lineages differentiation is unclear. Expression data from hematopoietic stem cells plated on OP9 stroma expressing or not the Notch ligand Delta-like1. Results provide insight into the role of Notch signalling in megakaryocyte fate specification. Keywords: Gene expression array-based (RNA / in situ oligonucleotide)

2009-06-02 | GSE11723 | GEO

GATA3 restrains Notch signaling activity and represses NK cell development to induce human T cell commitment following Notch-induced T-lineage specification (ChIP-Seq)

2016-04-06 | GSE71751 | GEO