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Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

ABSTRACT: We found that JUN expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN, we worked with primary human fibrotic lung fibroblasts that have normal or Knock-out levels of JUN expression and performed ATAC-seq analysis in both of them. Meanwhile we also modified primary human normal lung fibroblasts with or without JUN over-expression induction, then processed ATAC-seq and ChIP-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE114844 | GEO | 2020/04/27

REPOSITORIES: GEO

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Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

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Mouse Embryonic Stem Cells Resist c-Jun induced Differentiation in Suspension

Project description:The oncogene c-Jun plays a key role in development and cancer. Yet, its role in cell fate decision remains poorly understood at the molecular level. Here we report that c-Jun confers different fate decisions upon mouse embryonic stem cells (mESCs) in adhesion vs suspension. We developed a Tet-on system for temporal induction of c-Jun expression by Doxycycline treatment in mESCs. We show that mESCs carrying the inducible c-Jun TetOn remain pluripotent and grow slowly in suspension with induction of c-Jun, while undergoing differentiation with normal proliferative potentials in adherence upon c-Jun induction. Apparently, c-Jun pushes mESCs in suspension into cell cycle arrest at G1/S, through the induction of Cdkn1a/b and Cdkn2/a/b/c. Despite cell cycle arrest, they can re-enter cell cycle upon plating on adhesive surface and grow into typical mESC colonies albeit at lower efficiency. These results demonstrate that mESCs respond to c-Jun differently in suspension or adherence. Our results suggest that cells in suspension may be more resistant to differentiation than in adherence.

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Genome-wide maps of H3K27ac, H3K4me1, JUN and p-JUN in JUN overexpressed or JUN inactivated fibroblasts

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