Project description:We performed whole genome expression analysis of Kit+ derived from wild type C57B/L6 Mouse bone marrow cells Trabsduced with control vector and CSF3R mutants by RNA seq.
Project description:The single cell level Paneth cell transcriptome under gnotobiotic condition has not been resolved. How gut microbiome modulates Paneth cell transcriptome at single cell level in germ-free mice was not known. We used a flow cytometry method to isolate highly pure ileal Paneth cells from germ free (GF) Paneth cell reporter mice (Lyz1-3'UTR-IRES-CreER) and from exGF Paneth cell reporter mice that were transplanted with wild type C57B/l6 mouse gut microbiota (exGF+B6M). These isolated Paneth cells were subjected to single cell RNA sequencing by 10xGenomics.
Project description:Purpose: The goals of this study are to study the expression of Sfxn3 in C57B/L6 mouse retina and retinal cell types Methods: Library prepared followed by 10X Genomics standard protocol. Transcriptome were generated by high throughput sequencing
Project description:Comparison of gene expression in the stromal cell compartment (Lineage negative, CD45 negative bone marrow cells) of C57B/L6 and B6.SJL (Ly5.1) mice. duplicate samples were analyzed per strain (two biological replicates) and each of the two samples was pooled from 5 mice
Project description:To characterize the effect of microbiota on global gene expression in the distal small intestine during postnatal gut development we employed mouse models with experimental colonization by intestinal microbiota. Using microarray analysis to assess global gene expression in ileal mucosa at the critical stage of intestinal development /maturation associated with weaning, and asking how expression is affected by microbial colonization In the study presented here, preweaned and postweaned GF, SPF mouse small intestinal total RNAs were used. Also, 3-week-old gnotobiotic mouse as well as GF mouse small intestinal RNAs were used.
Project description:We profiled transcriptome and chromatin landscapes in jejunal mouse intestinal epithelial cells (IECs) from mice reared in the absence (Germ Free or GF) or presence (Conventionalized or CV) of microbiota. We show that microbiota colonization results in changes in histone modifications at hundreds of enhancers that are associated with microbiota-regulated genes. Furthermore, we show that microbiota colonization is associated with a drastic genome-wide reduction in Hnf4a and Hnf4g binding.
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs. mRNA and accessible chromatin (DNase-seq) profiles from colonic and ileal IECs were compared between conventionally-raised (CR), germ-free (GF), and conventionalized (CV) C57BL/6 mice.
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury
