RNA-seq analysis of WT and CARD11 point mutation mouse spleen B cells
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ABSTRACT:
PROVIDER: PRJNA562773 | ENA |
REPOSITORIES: ENA
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Project description:In order to investigate the molecular mechanism of CARD11 in immune cell system, we applied the RNA-seq analysis using RNA isolated from WT and CARD11 mutant (E134G and K215M) mouse spleen B cells. By comparing the transcriptome files, we found some different expressed gene involved in due to the CARD11 point mutation and in vitro RT-PCR had confirmed this result.
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Project description:Regeneration of differentiated tissue in mammals is rare. In an effort to identify genes that affect the healing process, we screened G3 mice containing germline point mutations for closure of an ear punch wound. One particular line was identified with a heritable hole closure phenotype containing differentiated tissue. Mapping and sequencing efforts revealed that the mutant mice harbor a R244Q point mutation coded by the TGFBR1 gene which leads to enhanced signaling activity in a reporter gene assay. Although there was no obvious effect on the immune system, bone marrow stromal cells from the mutant mice revealed accelerated chondrogenesis, mimicking the in vivo development of cartilage islands in the regenerated ears. This genetically well-defined mouse model should help to further dissect the role of TGF-beta signaling in vertebrate healing and regeneration. Keywords: treatment and time course in wt and mutant samples
2011-07-11 | GSE14523 | GEO
Project description:Regeneration of differentiated tissue in mammals is rare. In an effort to identify genes that affect the healing process, we screened G3 mice containing germline point mutations for closure of an ear punch wound. One particular line was identified with a heritable hole closure phenotype containing differentiated tissue. Mapping and sequencing efforts revealed that the mutant mice harbor a R244Q point mutation coded by the TGFBR1 gene which leads to enhanced signaling activity in a reporter gene assay. Although there was no obvious effect on the immune system, bone marrow stromal cells from the mutant mice revealed accelerated chondrogenesis, mimicking the in vivo development of cartilage islands in the regenerated ears. This genetically well-defined mouse model should help to further dissect the role of TGF-beta signaling in vertebrate healing and regeneration. Keywords: treatment and time course in wt and mutant samples TGFb or vehicle treatment at different time points in mouse embryonic fibroblasts from wildtype and TGFb1 mutant (heterozygous and homozygous) mice. Mutant is constitutively active.
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Project description:Analysis of the transcriptome pattern of spleen after maralia infection in WT and miR-155 KO mice.
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Project description:We describe the use of saturation genome editing to measure the effects of CARD11 variants on protein function, splicing and lymphoma cell survival. We find the results to predict the clinical effects of the variants.
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Project description:The immune system plays a critical role in inflammation by initiating responses to infection or tissue damage. NF-κB pathway plays a key role in inflammation and innate immunity, as well as other cellular activities. Furthermore, dysregulation of this well-choreographed pathway has been observed in many diseases, including cancer. CARD11 is a key molecule in the BCL-10, MALT1 (CBM) complex which is involved in transducing the signal downstream of the NF-κB pathway. This study aims to understand how overexpression of CARD11 adversely affects the prognosis in colorectal cancer (CRC) as it progresses towards aggressive form of the disease and the role that CARD11 plays in modulating the immune response across the different stages of CRC. To identify some of the cellular pathways activated as a result of CARD11, whole tran-scriptomics analysis was carried comparing the transcriptomic profile of CARD11-overexpressed HCT-116 and HT-29 CRC cell lines with empty vector-transfected cell lines as well as comparing adenoma and carcinoma CRC patients with CARD11- and CARD11+ expression. The whole tran-scriptomics and bioinformatics analysis results strongly suggested that CARD11 appears to play a key role in CRC progression. Absolute Gene Set Enrichment Analysis (absGSEA) on HCT-116 transcriptomics data showed that CARD11 overexpression promotes cell growth, and tissue re-modeling as well as enhancing the cell’s immune response. Some of the underlying genes in-volved in such processes through co-expression with CARD11 include EP300, KDM5A, HIF1A, NFKBIZ, and DUSP1. Results for HT-29 showed that CARD11 overexpression induces chemotaxis and ECM organization pathways through co-expression of IL1RN, MDK, and SPP1 as well as var-ious chemokines including CXCL1, CXCL3 and CCL22 which were shown to contribute to the more invasive stage of CRC. For patients, the adenoma patients include genes related to tumour immune microenvironment such as IL6ST, genes related to collagen family as well as other genes related to transition to CRC such as GLI3 and PIEZO2. While carcinoma patients show dramatic increase in the expression of MAPK8IP2 in CARD11+ carcinoma patients in addition to other genes related to cancer processes including EMB, EPHB6, and CPEB4. Taken together, the results show that CARD11 overexpression contributes to the progression of CRC through modu-lation of various tumour immune microenvironment pathways and activation of cancer path-ways possibly via the dysregulation of NF-κB. To our knowledge, this is probably the first study that investigates the role of CARD11 in CRC and the genes and pathways associated with CARD11 overexpression may provide insights into the early diagnostic and possible therapeutic targets for CRC.
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Project description:From lymphoblastoid cell lines derived from two homozygous CARD11-deficient patients and two heterozygous parents of the first patient, we performed differential expression analysis, gene set enrichment, and pathway analyses by RNA-Seq to demonstrate impaired activation of critical immune pathways.
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Project description:Inflammatory bowel disease is characterized by chronic relapsing idiopathic inflammation of the gastrointestinal tract and persistent inflammation. Studies focusing on the immune-regulatory function of reactive oxygen species (ROS) are still largely missing. In this study, we analyzed an ROS-deficient mouse model leading to colon adenocarcinoma. Colitis was induced with dextran sulfate sodium (DSS) supplied via the drinking water in wild-type (WT) and Ncf1-mutant (Ncf1) B10.Q mice using two different protocols, one mimicking recovery after acute colitis and another simulating chronic colitis. Disease progression was monitored by evaluation of clinical parameters, histopathological analysis, and the blood serum metabolome using 1H nuclear magnetic resonance spectroscopy. At each experimental time point, colons and spleens from some mice were removed for histopathological analysis and internal clinical parameters. Clinical scores for weight variation, stool consistency, colorectal bleeding, colon length, and spleen weight were significantly worse for Ncf1 than for WT mice. Ncf1 mice with only a 7-day exposure to DSS followed by a 14-day resting period developed colonic distal high-grade dysplasia in contrast to the low-grade dysplasia found in the colon of WT mice. After a 21-day resting period, there was still β-catenin-rich inflammatory infiltration in the Ncf1 mice together with high-grade dysplasia and invasive well-differentiated adenocarcinoma, while in the WT mice, high-grade dysplasia was prominent without malignant invasion and only low inflammation. Although exposure to DSS generated less severe histopathological changes in the WT group, the blood serum metabolome revealed an increased fatty acid content with moderate-to-strong correlations to inflammation score, weight variation, colon length, and spleen weight. Ncf1 mice also displayed a similar pattern but with lower coefficients and showed consistently lower glucose and/or higher lactate levels which correlated with inflammation score, weight variation, and spleen weight. In our novel, DSS-induced colitis animal model, the lack of an oxidative burst ROS was sufficient to develop adenocarcinoma, and display altered blood plasma metabolic and lipid profiles. Thus, oxidative burst seems to be necessary to prevent evolution toward cancer and may confer a protective role in a ROS-mediated self-control mechanism.
2019-05-22 | MTBLS593 | MetaboLights