This SuperSeries is composed of the SubSeries listed below.
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis.
Specimen part
View SamplesThe development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3IEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3IEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3IEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3IEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis.
Specimen part
View SamplesThe development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3IEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3IEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3IEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3IEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis.
Specimen part
View SamplesComparison between in vitro transcription- and cDNA-mediated annealing, selection and ligation (DASL)-based assays on brain-specific reference RNA, and postmortem frozen and formalin fixed brain tissue from autistic and control cases. Investigation of data preprocessing techniques for DASL-assayed RNA samples from frozen brain tissue.
Preprocessing and Quality Control Strategies for Illumina DASL Assay-Based Brain Gene Expression Studies with Semi-Degraded Samples.
Specimen part, Disease
View SamplesProper cortical development relies on the balance of neuronal migration and proliferation. We investigated the gene expression differences of mouse knock-outs for Lissencephaly in humans.
Global developmental gene expression and pathway analysis of normal brain development and mouse models of human neuronal migration defects.
Specimen part
View SamplesWe report RNA-Seq experiments of whole eye tissues from A/J, BALB/c, and C57BL/6 background mice. Overall design: Examine ocular tissue from 3 different background mice that display varying rates of retinal degeneration.
Transcriptome analysis reveals rod/cone photoreceptor specific signatures across mammalian retinas.
Sex, Age, Specimen part, Cell line, Subject
View SamplesWe report RNA-Seq experiments of eye and retinal tissues from WT and RHO KO mice Overall design: Examine ocular tissue from different mouse genotypes
Transcriptome analysis reveals rod/cone photoreceptor specific signatures across mammalian retinas.
Specimen part, Cell line, Subject
View SamplesWe report RNA-Seq experiments of whole eye tissues from C57BL/6J background mice at 1.5 h and 9.0 h after light onset to better understand photoreceptor phagocytosis Overall design: Examine ocular tissue from mice at different time points
Transcriptome analysis reveals rod/cone photoreceptor specific signatures across mammalian retinas.
Specimen part, Cell line, Subject, Time
View SamplesRIPK4 but not the related kinases RIPK1, RIPK2, and RIPK3 caused similar transcriptional changes to Wnt3a. Overall design: PA1 cells were transfected by 8ug RIPK1, RIPK2, RIPK3, or RIPK4 for 48h, RNA were extracted and sequenced.
Phosphorylation of Dishevelled by protein kinase RIPK4 regulates Wnt signaling.
Cell line, Subject
View SamplesHeterogeneity of meningeal cortical cells was deciphered on the molecular level using single cell RNA seq Overall design: RNA sequencing of 179 meningeal cortical cells isolated from naive wild-type mice
Neurogenic Radial Glia-like Cells in Meninges Migrate and Differentiate into Functionally Integrated Neurons in the Neonatal Cortex.
Sex, Specimen part, Subject
View Samples