Irf6 wildtype and knock out ATAC-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA524711 | ENA |
REPOSITORIES: ENA
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Project description:The integrity of the mammalian epidermis is essential for organism survival, and it depends on a balance of proliferation and differentiation in the resident stem cell population. The kinase Ripk4 and the transcription factor Irf6 are mutated in severe developmental syndromes in humans, and mice lacking these genes display epidermal hyperproliferation and soft tissue fusions, resulting in neonatal lethality. However, the mechanism by which these genes control epidermal differentiation in vivo is unknown. By generating various mouse knock-out and knock-in strains we demonstrate that in vivo the role of Ripk4 in development is dependent on its kinase activity, Ripk4 and Irf6 function cell autonomously in the epidermis,Ripk4 and Irf6 lie on a linear pathway and phosphorylation of Irf6 on Serine413 and Serine424 is essential to prime it for activation. This priming then allows Ripk4 to phosphorylate Irf6 on Serine90, which ensures Irf6 activation. We then use RNA-seq, ChIP-seq and ATAC-seq analysis to define the global transcriptional targets of Irf6 in epidermal differentiation. Collectively, our results explain how Ripk4 activates Irf6, and how this pathway ensures epidermal differentiation and a functional barrier. This is crucial for understanding the etiology of developmental syndromes that are characterized by orofacial, skin and genital abnormalities.
2019-08-29 | GSE127341 | GEO
Project description:Irf6 wildtype and knock out ChIP-seq
| PRJNA524709 | ENA
Project description:The integrity of the mammalian epidermis is essential for organism survival, and it depends on a balance of proliferation and differentiation in the resident stem cell population. The kinase Ripk4 and the transcription factor Irf6 are mutated in severe developmental syndromes in humans, and mice lacking these genes display epidermal hyperproliferation and soft tissue fusions, resulting in neonatal lethality. However, the mechanism by which these genes control epidermal differentiation in vivo is unknown. By generating various mouse knock-out and knock-in strains we demonstrate that in vivo the role of Ripk4 in development is dependent on its kinase activity, Ripk4 and Irf6 function cell autonomously in the epidermis,Ripk4 and Irf6 lie on a linear pathway and phosphorylation of Irf6 on Serine413 and Serine424 is essential to prime it for activation. This priming then allows Ripk4 to phosphorylate Irf6 on Serine90, which ensures Irf6 activation. We then use RNA-seq, ChIP-seq and ATAC-seq analysis to define the global transcriptional targets of Irf6 in epidermal differentiation. Collectively, our results explain how Ripk4 activates Irf6, and how this pathway ensures epidermal differentiation and a functional barrier. This is crucial for understanding the etiology of developmental syndromes that are characterized by orofacial, skin and genital abnormalities.
2019-08-29 | GSE127338 | GEO
Project description:The integrity of the mammalian epidermis is essential for organism survival, and it depends on a balance of proliferation and differentiation in the resident stem cell population. The kinase Ripk4 and the transcription factor Irf6 are mutated in severe developmental syndromes in humans, and mice lacking these genes display epidermal hyperproliferation and soft tissue fusions, resulting in neonatal lethality. However, the mechanism by which these genes control epidermal differentiation in vivo is unknown. By generating various mouse knock-out and knock-in strains we demonstrate that in vivo the role of Ripk4 in development is dependent on its kinase activity, Ripk4 and Irf6 function cell autonomously in the epidermis,Ripk4 and Irf6 lie on a linear pathway and phosphorylation of Irf6 on Serine413 and Serine424 is essential to prime it for activation. This priming then allows Ripk4 to phosphorylate Irf6 on Serine90, which ensures Irf6 activation. We then use RNA-seq, ChIP-seq and ATAC-seq analysis to define the global transcriptional targets of Irf6 in epidermal differentiation. Collectively, our results explain how Ripk4 activates Irf6, and how this pathway ensures epidermal differentiation and a functional barrier. This is crucial for understanding the etiology of developmental syndromes that are characterized by orofacial, skin and genital abnormalities.
2019-08-29 | GSE124047 | GEO
Project description:The integrity of the mammalian epidermis is essential for organism survival, and it depends on a balance of proliferation and differentiation in the resident stem cell population. The kinase Ripk4 and the transcription factor Irf6 are mutated in severe developmental syndromes in humans, and mice lacking these genes display epidermal hyperproliferation and soft tissue fusions, resulting in neonatal lethality. However, the mechanism by which these genes control epidermal differentiation in vivo is unknown. By generating various mouse knock-out and knock-in strains we demonstrate that in vivo the role of Ripk4 in development is dependent on its kinase activity, Ripk4 and Irf6 function cell autonomously in the epidermis,Ripk4 and Irf6 lie on a linear pathway and phosphorylation of Irf6 on Serine413 and Serine424 is essential to prime it for activation. This priming then allows Ripk4 to phosphorylate Irf6 on Serine90, which ensures Irf6 activation. We then use RNA-seq, ChIP-seq and ATAC-seq analysis to define the global transcriptional targets of Irf6 in epidermal differentiation. Collectively, our results explain how Ripk4 activates Irf6, and how this pathway ensures epidermal differentiation and a functional barrier. This is crucial for understanding the etiology of developmental syndromes that are characterized by orofacial, skin and genital abnormalities.
2019-08-29 | GSE124048 | GEO
Project description:Transcriptome profiling of murine liver from EndoV knock-out and wildtype mice
| PRJNA604842 | ENA
Project description:Goal: elucidate transcriptomic changes upon knock-out of components of the FERRY complex Methods: RNA extraction from HeLa wildtype and fy-1, fy-2, fy-4 and fy-5 knock-out celllines and subsequent RNASeq Results: We observed differences in the transcriptome of all four knock-out cell lines Conclusions: In the Analysis we focused on genes that were differentially expressed in all four KO cell lines or upon KO of fy-1 and fy-2.
2023-04-27 | GSE230114 | GEO
Project description:To investigate the functional importance of a nucleoside transporter, the mENT1 (Slc29a1) was knocked out in mice. The gene expression profile was compared between wildtype and mENT1 knock out mice in two tissues.
2011-04-27 | GSE22565 | GEO
Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.
2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress
Project description:(1) While it is known that redox-regulation in chloroplasts is vital for functional photosynthesis, the interplay of different redox-cascades in balancing reactive oxygen species (ROS) with metabolic regulation via thiol switching is still partly unresolved. We investigate the importance of the glutathione reductase isoform maintaining a highly reducing stromal glutathione redox potential (EGSH). (2) Using the model moss Physcomitrella patens, we knocked-out the plastid/mitochondrial GR isoform. We generated a sensor line expressing plastid-targeted redox-sensitive GFP to monitor stromal EGSH in vivo, and compared protein abundances between wildtype (WT) and Δgr1 knock-out mutants by a metabolic labelling approach. (3) On the organelle level, we find that the absence of PpGR1 leads to a shift of stromal EGSH to less reducing values that is not rescued in the light, whereas WT EGSH was clearly responsive to light. On the plant level, growth and photosynthetic performance were decreased with increasing light intensities while ascorbate and zeaxanthin levels were elevated. Proteomics showed an induction of proteins involved in plastid protein repair and degradation. (4) Our results indicate a limited cross-talk between plastid thioredoxin and glutathione redox systems and show that glutathione reductase is necessary for efficient photosynthesis under stress and non-stress conditions.
2020-05-06 | PXD012843 | Pride