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The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

ABSTRACT: The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

PROVIDER: PRJNA546585 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9204660.fastq.gz	Fastqsanger.gz
	SRR9204661.fastq.gz	Fastqsanger.gz
	SRR9204662.fastq.gz	Fastqsanger.gz
	SRR9204654.fastq.gz	Fastqsanger.gz
	SRR9204655.fastq.gz	Fastqsanger.gz

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The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

Project description:The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

| PRJNA545221 | ENA

The WT1-like transcription factor Klumpfuss maintains lineage commitment of enterocyte progenitors in the Drosophila intestine.

Project description:In adult epithelial stem cell lineages, the precise differentiation of daughter cells is critical to maintain tissue homeostasis. Notch signaling controls the choice between absorptive and entero-endocrine cell differentiation in both the mammalian small intestine and the Drosophila midgut, yet how Notch promotes lineage restriction remains unclear. Here, we describe a role for the transcription factor Klumpfuss (Klu) in restricting the fate of enteroblasts (EBs) in the Drosophila intestine. Klu is induced in Notch-positive EBs and its activity restricts cell fate towards the enterocyte (EC) lineage. Transcriptomics and DamID profiling show that Klu suppresses enteroendocrine (EE) fate by repressing the action of the proneural gene Scute, which is essential for EE differentiation. Loss of Klu results in differentiation of EBs into EE cells. Our findings provide mechanistic insight into how lineage commitment in progenitor cell differentiation can be ensured downstream of initial specification cues.

| S-EPMC6739418 | biostudies-literature

The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

Project description:RNA-Seq experiment of sorted Esg+ stem-progenitors expressing either RNA (kluRNAi) against Klu or overexpression of klu (UAS-klu)

2019-07-26 | GSE132243 | GEO

The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

Project description:DamID-Seq experiment with Kllu-Dam

2019-05-30 | GSE131878 | GEO

Histone Variant H2A.X Plays Novel Roles in Cell Lineage Commitment and Genomic Stability in ESC and iPSC

Project description:Herein, we demonstrated that the cell lineage commitment is unexpectedly regulated by the novel functions of H2A.X, a histone variant which was only well-known for its role in genome integrity maintenance previously. Surprisingly, only in ESCs but not differentiated cells, H2A.X is specifically targeted to genomic regions encoding early embryonic and extra-embryonic lineage genes to repress their expression. In addition, H2A.X is also enriched at genomic regions sensitive to replication stress and maintains genomic stability thereat. Most interestingly, faithful H2A.X deposition plays critical roles in maintaining both cell lineage commitment and genome integrity in iPSC. In iPSC lines which support the development of "all-iPS" animals, H2A.X deposition faithfully recapitulates the ESC pattern and therefore, the genome stability and cell lineage commitment are maintained. In iPSC lines that fail to support embryonic development, defective H2A.X depositions result in aberrant upregulation of early embryonic and extra-embryonic lineage genes and H2A.X-dependent genome instability. mRNA-Seq of WT ESC and H2A.X KO ESC; and 4N+, 4N- iPSC.

2014-09-07 | E-GEOD-49147 | biostudies-arrayexpress

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.

2016-10-24 | MSV000080283 | MassIVE

Epigenome regulation during epidermal lineage commitment

Project description:Epigenome regulation during epidermal lineage commitment

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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

Identification of DNA Methylation Markers for Lineage Commitment of in vitro Hepatogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE25046: Identification of DNA Methylation Markers for Lineage Commitment of in vitro Hepatogenesis [mRNA profiling] GSE25047: Identification of DNA Methylation Markers for Lineage Commitment of in vitro Hepatogenesis [methylation profiling] Refer to individual Series

2011-11-25 | E-GEOD-25048 | biostudies-arrayexpress

Histone Variant H2A.X Plays Novel Roles in Cell Lineage Commitment and Genomic Stability in ESC and iPSC

2014-09-07 | GSE49147 | GEO