Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1030552 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Emerging and neglected pathogens pose challenges as their biology is frequently poorly understood, and genetic tools often do not exist to manipulate them. Organism agnostic sequencing technologies offer a promising approach to understand the molecular processes underlying these diseases. Here we apply dual RNA-seq to Orientia tsutsugamushi (Ot), the obligate intracellular causative agent of the vector-borne human disease scrub typhus. Half the Ot genome is composed of repetitive DNA, and there is minimal collinearity in gene order between strains. Integrating RNA-seq, comparative genomics, proteomics, and machine learning, we investigated the transcriptional architecture of Ot, including operon structure and non-coding RNAs, and found evidence for wide-spread post-transcriptional antisense regulation. We compared the host response to two clinical isolates and identified distinct immune response networks that are up-regulated in response to each strain, leading to predictions of relative virulence which were confirmed in a mouse infection model. Thus, dual RNA-seq can reveal the biology and host-pathogen interactions of a poorly characterized and genetically intractable organism such as Ot.
2020-06-05 | PXD017956 | JPOST Repository
Project description:Groups of samples used in Microarray and comparative genomics-based identification of genes and gene regulatory regions of the mouse immune system profiles. Keywords: other
2010-05-03 | GSE2168 | GEO
Project description:Groups of samples used in Microarray and comparative genomics-based identification of genes and gene regulatory regions of the mouse immune system profiles.
2010-06-10 | E-GEOD-2168 | biostudies-arrayexpress
Project description:We previously identified Tbc1d23 as a candidate novel regulator of innate immunity using comparative genomics RNAi screens in C. elegans and mouse macrophages. Using mice with an engineered knockout mutation in Tbc1d23 and macrophages engineered to overexpress Tbc1d23, we now show that Tbc1d23 is a general but not universal inhibitor of the innate immune response, inhibiting multiple Toll-like receptor (TLR) and Dectin signaling pathways but not NOD signaling pathways. Tbc1d23 likely acts downstream of the TLR signaling adaptors MyD88 and Trif and upstream of the transcription factor XBP1. Importantly, like XBP1, Tbc1d23 affects the maintenance but not initiation of inflammatory cytokine production induced by lipopolysaccharide (LPS). The identification of a novel temporal regulator of innate immunity signaling validates the comparative genomics approach for innate immunity gene discovery.
2012-04-04 | GSE30840 | GEO
Project description:We previously identified Tbc1d23 as a candidate novel regulator of innate immunity using comparative genomics RNAi screens in C. elegans and mouse macrophages. Using mice with an engineered knockout mutation in Tbc1d23 and macrophages engineered to overexpress Tbc1d23, we now show that Tbc1d23 is a general but not universal inhibitor of the innate immune response, inhibiting multiple Toll-like receptor (TLR) and Dectin signaling pathways but not NOD signaling pathways. Tbc1d23 likely acts downstream of the TLR signaling adaptors MyD88 and Trif and upstream of the transcription factor XBP1. Importantly, like XBP1, Tbc1d23 affects the maintenance but not initiation of inflammatory cytokine production induced by lipopolysaccharide (LPS). The identification of a novel temporal regulator of innate immunity signaling validates the comparative genomics approach for innate immunity gene discovery. Total of 24 samples; Tbc1d23-overexpressing line and control line; 0, 1, 3, and 5 hour LPS treatment; 3 biological replicates per group
2012-04-03 | E-GEOD-30840 | biostudies-arrayexpress
Project description:Interventions: Case series:N/A
Primary outcome(s): Serum immune cytokines;Blood immune cells;SCFAs of bacterial metabolites;Gut microbial genomics;Metabolic function of intestinal microorganism
Study Design: Sequential
| 2706719 | ecrin-mdr-crc