Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1040292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26864400_1.fastq.gz | Fastqsanger.gz | |||
| SRR26864400_2.fastq.gz | Fastqsanger.gz | |||
| SRR26864401_1.fastq.gz | Fastqsanger.gz | |||
| SRR26864401_2.fastq.gz | Fastqsanger.gz | |||
| SRR26864402_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 182 |
Similar Datasets
Project description:Individual leaf microbiota tunes a genetic regulatory network to promote leaf growth
| PRJEB79411 | ENA
Project description:: Individual leaf microbiota tunes a genetic regulatory network to promote leaf growth
| PRJEB79409 | ENA
Project description:Molecular adaptation of the intestinal mucosa occurs during microbial conventionalization to maintain a balanced immune response. However, the genetic regulation of such adaptation is obscure. Here, combined analysis of germ free and conventionalized mice revealed that the major molecular adaptations were initiated at day 4 of conventionalization with a strong induction of innate immune functions followed by stimulation of adaptive immune functions. We identified central regulatory genes and reconstructed a common regulatory network that appeared to be sufficient to regulate the dynamic adaptation of the intestinal mucosa to the colonizing microbiota. The majority of the genes within this regulatory network play roles in mucosal inflammatory diseases in mouse and human. We propose that the identified central regulatory network may serve as a genetic signature for control of intestinal homeostasis in healthy mice and may help to unravel the genetic basis of pathway dysregulation in human intestinal inflammatory diseases. Expression profiling of jejunum, ileum, and colon tissue from germ-free and colonized mice at day 1,2,4,8,16 and 30.
2012-07-10 | E-GEOD-32513 | biostudies-arrayexpress
Project description:Resident microorganisms (microbiota) have far-reaching effects on the biology of their animal hosts, with major consequences for the host’s health and fitness. Some of these effects can be explained by microbial impacts on the expression of individual genes but a full understanding of microbiota-dependent gene regulation requires analysis of the overall architecture of the host transcriptome. In this study, we investigated the impact of the microbiota on the global structure of the transcriptome of Drosophila. Our transcriptomic analysis of 17 Drosophila lines representative of the global genetic diversity of this species yielded a total of 11 transcriptional modules of co-expressed genes. For 7 of these modules, the strength of the transcriptional network (defined as gene-gene coexpression) differed significantly between flies bearing a defined gut microbiota (gnotobiotic flies) and flies reared under microbiologically-sterile conditions (axenic flies). Furthermore, the network structure was uniformly stronger in these microbiota-dependent modules than in both the microbiota-independent modules in gnotobiotic flies and all modules in axenic flies, indicating that the presence of the microbiota tightens gene regulation in a subset of the transcriptome. The genes constituting the microbiota-dependent transcriptional modules include regulators of growth, metabolism and neurophysiology, previously implicated in mediating phenotypic effects of microbiota on Drosophila phenotype. Together these results provide the key first evidence that the microbiota strengthens the co-expression of genesin specific networks of functionally-related transcripts relative to the animal’s intrinsic baseline level of co-expression. Our system-wide analysis demonstrates that the presence of microbiota enhances the structure of the transcriptional network in the animal host. This finding has potentially major implications for understanding of the mechanisms by which microbiota affect host health and fitness, and the ways in which hosts and their resident microbiota coevolve.
2016-12-31 | GSE87818 | GEO
Project description:Disruptions of microbiota composition by factors such as genetics have been suggested to be critical contributing factors to the growth of the worldwide epidemics of chronic illness such as metabolic diseases. IL-35-producing regulatory B and T regulatory cells are critical regulators to these illnesses. Whether microbiota-derived metabolites can regulate these IL-35+ cells maintain elusive. Here, we found gut genetic factor Reg4 associated lactobacillus could promote the generation of IL-35+ B cells through producing 3-idoleacetic acid (IAA). HuREG4IEC tg mice had markedly accumulation of IL-35+ not only in adipose tissues but also in colon tissues; whereas significantly decreased IL-35+ cells in adipose tissues and colon tissues could be detected in Reg4 KO mice. On the mechanism, IAA-mediated IL35+ B cells was through PXR), RXR and CAR in the presence of LPS. PXR KO, CAR KO and NF-B KO mice impaired the generation of IAA- IL-35+B cells. Interestingly, lower levels of IAA and IL-35 were also detected in the peripheral blood of individuals with obesity. Thus, IAA is a factor to promote the generation of IL-35+B cells to impede the development of obesity.
2021-02-08 | GSE166316 | GEO