Global expression analysis of neural crest-like skin-derived precursors (SKPs) and Sox2-positive follicle dermal cells that SKPs originate from.
SKPs derive from hair follicle precursors and exhibit properties of adult dermal stem cells.
Specimen part
View SamplesPro-regenerative macrophages are well known for their role in promoting tissue repair, however in nerve injury their role in promoting regenerative events is not well defined. Macrophage-targeted RNAseq revealed that macrophages expressed an array of ligands post nerve injury that interact with the injury environement to regulate regeneration. Overall design: RNAseq experiment was performed on FACS-collected cells obtained from the nerves of adult female mice (n=7-8 per time point at Day 3 and 8 post-nerve injury) from a double macrophage reporter (Cx3cr1-GFP/Ccr2-RFP) mouse line (stock no.: 017586; stock No.: 005582, Jackson Laboratories). Samples were pooled to obtain 2 RNAseq sample replicates per time point. Monocytes were also included as a reference.
Macrophages Regulate Schwann Cell Maturation after Nerve Injury.
Sex, Age, Specimen part, Cell line, Subject
View SamplesSkin-derived precursors (SKPs) are multipotent dermal stem cells that reside within a hair follicle niche and that share properties with embryonic neural crest precursors. Here, we have asked whether SKPs and their endogenous dermal precursors originate from the neural crest or whether, like the dermis itself, they originate from multiple developmental origins. To do this, we used two different mouse Cre lines that allow us to perform lineage tracing: Wnt1-cre, which targets cells deriving from the neural crest, and Myf5-cre, which targets cells of a somite origin. By crossing these Cre lines to reporter mice, we show that the endogenous follicle-associated dermal precursors in the face derive from the neural crest, and those in the dorsal trunk derive from the somites, as do the SKPs they generate. In spite of these different developmental origins, SKPs from these two locations are functionally similar, even with regard to their ability to differentiate into Schwann cells, a cell type only thought to be generated from the neural crest. Analysis of global gene expression using microarrays confirmed that facial and dorsal SKPs exhibit a very high degree of similarity, and that they are also very similar to SKPs derived from ventral dermis, which has a lateral plate origin. However, these developmentally-distinct SKPs also retain differential expression of a small number of genes that reflect their developmental origins. Thus, an adult neural crest-like dermal precursor can be generated from a non-neural crest origin, a finding with broad implications for the many neuroendocrine cells in the body.
Convergent genesis of an adult neural crest-like dermal stem cell from distinct developmental origins.
Specimen part
View SamplesComparison of gene expression profile of HEK293 cells stably expressing a shRNA control (SilX-CT) or a shRNA against BAHD1 (SilX-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line
View SamplesComparison of gene expression profile of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line, Treatment
View SamplesGene silencing via heterochromatin formation plays a major role in cell differentiation and maintenance of homeostasis. Here, we report the identification and characterization of a novel heterochromatinization factor in vertebrates, Bromo Adjacent Homology Domain-containing protein 1 (BAHD1). BAHD1 interacts with HP1, MBD1, HDAC5 and with several transcription factors. Through electron and immunofluorescence microscopy studies, we show that BAHD1 overexpression directs HP1 to specific nuclear sites and promotes formation of large heterochromatic domains, which lack acetyl histone H3 and are enriched in H3 trimethylated at lysine 27. Furthermore, ectopically expressed BAHD1 colocalizes with the heterochromatic X inactive chromosome. As highlighted by whole genome microarray analysis of BAHD1 knock down cells, BAHD1 represses several proliferation and survival genes and in particular, the insulin-like growth factor II gene (IGF2). BAHD1 specifically binds the CpG-rich P3 promoter of IGF2. This region contains DNA binding sequences for the transcription factor SP1, with which BAHD1 co-immunoprecipitates. Collectively, these findings provide evidence that BAHD1 acts as a silencer by recruiting proteins that coordinate heterochromatin assembly at specific sites in the genome.
Human BAHD1 promotes heterochromatic gene silencing.
Cell line
View SamplesAll highly and poorly permeable metastases from the same mouse brain were collected by laser capture microdissection. Total RNA from both metastatic lesions and immediate microenvironment was isolated from 5 mice bearing 231-BR metastases. As control 4 healthy mouse brains were included.
Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Role of the BAHD1 Chromatin-Repressive Complex in Placental Development and Regulation of Steroid Metabolism.
Specimen part, Disease, Cell line, Treatment
View SamplesTo identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d).
ICL-induced miR139-3p and miR199a-3p have opposite roles in hematopoietic cell expansion and leukemic transformation.
Age, Specimen part
View SamplesmRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated Overall design: mRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated
Murine Norovirus Infection Induces T<sub>H</sub>1 Inflammatory Responses to Dietary Antigens.
Age, Specimen part, Cell line, Subject
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