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Cloning and comparison of human P63+ progenitor cells from various lung diseases [bulkRNA-seq]

ABSTRACT: Cloning and comparison of human P63+ progenitor cells from various lung diseases [bulkRNA-seq]

PROVIDER: PRJNA1083475 | ENA |

REPOSITORIES: ENA

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Cloning and comparison of human P63+ progenitor cells from various lung diseases [bulkRNA-seq]

Project description:KRT5+P63+ progenitor cells located in the basal layer of the airway epithelium have been identified as a promising candidate for lung epithelium repair. To investigate P63+ progenitor cells in human, we cloned KRT5+P63+ progenitors from both healthy donors and patients with various lung diseases.

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Cell culture of p63 knock out and wild type bladder epithelial stem cell

Project description:Although there are several reports describing a stem cell fraction to form urothelium and lineage tracing studies in urinary bladder, it is still unclear about stem cells in mouse bladder epithelium. Here, we have established the cloning system of mouse stem cells from wild type and p63 knockout bladder. We isolated stem/progenitor cells from wild type and p63 knockout epithelium. From wild type bladder, we have cloned keratin 5-positive stem cells, and from p63 knockout epithelium, which loses basal cell fraction, we have cloned morphologically-distinct keratin 8 and claudin 3 positive stem cells, which may be reminiscent of intestinal metaplasia in bladder.

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Cloning and Variation of Ground State Intestinal Stem Cells

Project description:Despite major advances with embryonic and induced pluripotent stem cells or lineage-committed, p63-expressing stem cells of stratified epithelia, we know less about the indigenous stem cells of the gastrointestinal tract, pancreas, liver, and other columnar epithelia which collectively resist cloning in their elemental states. Here we demonstrate the cloning of highly immature epithelial stem cells from defined regions of the human intestine and colon. We show that single cell-derived pedigrees can be propagated indefinitely while often sustaining minimal copy number and sequence variation. Despite prolonged cultivation, these pedigrees from disparate regions of the intestinal tract respond to identical differentiation signals by formation of epithelia with eponymous structural and gene expression features. These data suggest developmental patterning of cell-autonomous commitment programs in stem cells that enforce specialization along the gastrointestinal tract and predict the utility of these cells in disease modeling and regenerative medicine.

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Chromatin modification is not a prerequisite for p63 binding but p63 binding can elicit chromatin remodeling

Project description:Transcription factor (TF) p63 is a master regulator playing critical roles in epidermal development and other cellular processes. Our lab’s previous research deciphered a distinct chromatin architecture at p63 bound site in keratinocytes. In order to figure out whether those chromatin modifications already exist before p63 binding, or p63 occupancy contributes to such chromatin marks, we built p63-expressing cell lines. We then obtained p63 bound regions in these overexpressing cell line, and looked at different histone marks at those sites before p63 occupancy. As shown in the results, before p63 binding, the targeting sites have barely detectable histone marks, indicating p63’s capability to approach unmodified chromatins. Moreover, there is no significant difference in chromatin marks between p63 bound sites and unbound sites when no p63 binding happens. Our in vivo findings were confirmed by examining p63 binding to unmodified nucleosomes in vitro, showing that histone modification is not indispensable for p63 binding but binding site positioning on nucleosome does play a role. Overall, our results suggest that histone modifications do not affect p63 binding, and p63 protein can bind to inaccessible, weakly modified chromatin regions in vivo.

2020-12-01 | GSE140329 | GEO

Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

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Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

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Genome-wide profiling of p63 binding sites identifies genes and regulatory elements for p63-related disorders

Project description:We identified p63 target genes and binding sites responsible for ectodermal defects by genome-wide profiling of p63 binding using ChIP-seq and expression analysis in human primary keratinocytes from patients with p63 mutations. As proof of principle, we identified a novel de novo microdeletion causing limb defects (SHFM1) that includes a p63 binding site functioning as a cis-regulatory element to control expression of the distally located DLX5/DLX6 genes essential for limb development. Our data demonstrate that target genes and regulatory elements detected in this study can serve as powerful tools to identify causative mutations of unresolved ectodermal disorders. ChIP-seq profiles of p63 in primary human keratinocytes established from two different normal individuals.

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Generation of patient-relevant p63 gene signature to identify novel oncogenes and tumor suppressors that contribute to HNSCC development and progression

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Genome-wide profiling of p63 binding sites identifies genes and regulatory elements for p63-related disorders

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