The intention of these gene expression analysis was to study host responses to an infection with Agrobacterium tumefaciens at different stages of crown gall development. Therefore the transcriptome of infected inflorescence stalk tissue and mature crown galls of Arabidopsis thaliana (WS-2) was determined of three different time points. These were compared with the transcriptome of mock-infected inflorescence stalk tissue (reference) of the same age. The following time points were analyzed: (i) three hours post inoculation, before the T-DNA is integrated into the host genome (ii) six days after inoculation when the T-DNA is present in the nucleus and the oncogenes are expressed in the host cell, and (iii) 35 days after inoculation when a mature tumors has developed. For the three-hour- (3hpi) and six-day- time point (6dpi) plants were infected with the virulent strain C58, harboring a T-DNA, or with strain GV3101, containing a disarmed Ti-plasmid. This allows discrimination between signals which derive from the bacterial pathogen and the T-DNA encoded oncogenes.
An integrated view of gene expression and solute profiles of Arabidopsis tumors: a genome-wide approach.
Specimen part
View SamplesThis study focuses on responses of the host plant to infection with Agrobacterium tumefaciens. Genome wide changes in gene expression were integrated with the alterations in metabolite levels three hours after inoculation of agrobacteria. Plants were infected with the virulent strain C58, harboring a T-DNA, or with strain GV3101, containing a disarmed Ti-plasmid. This allows discrimination between signals which derive from the bacterial pathogen and the T-DNA encoded genes.
An integrated view of gene expression and solute profiles of Arabidopsis tumors: a genome-wide approach.
Specimen part
View SamplesThis study focuses on responses of the host plant to infection and transformation with Agrobacterium tumefaciens. Genome wide changes in gene expression were integrated with the alterations in metabolite levels six days after inoculation of agrobacteria. Plants were infected with the virulent strain C58, harboring a T-DNA, or with strain GV3101, containing a disarmed Ti-plasmid. This allows discrimination between signals which derive from the bacterial pathogen and the T-DNA encoded genes.
An integrated view of gene expression and solute profiles of Arabidopsis tumors: a genome-wide approach.
Specimen part
View SamplesThis study describes physiological changes, morphological adaptations and the regulation of pathogen defense responses in Arabidopsis crown galls. Crown gall development was induced on intact plants under most natural conditions with Agrobacterium tumefaciens. Differential gene expression and the metabolite pattern was determined by comparing crown galls with mock-inoculated inflorescence stalk segments of the same age.
An integrated view of gene expression and solute profiles of Arabidopsis tumors: a genome-wide approach.
Specimen part
View SamplesAn understanding of the mechanisms regulating white adipose tissue (WAT) formation is key for developing of new tools to treat obesity and its related diseases. Here, we identify DEPTOR as a positive regulator of adipogenesis whose expression is associated with obesity. In a polygenic mouse model of obesity/leanness, Deptor is part of the Fob3a QTL linked to obesity and we fine that Deptor is the highest priority candidate gene regulating WAT accumulation in this model. Using a doxycycline-inducible mouse model for Deptor overexpression, we confirmed that Deptor promotes WAT expansion in vivo. DEPTOR expression is elevated in WAT of obese humans and strongly correlates with the degree of obesity. We show that DEPTOR is induced during adipogenesis and that its overexpression cell-autonomously promotes, while its suppression blocks, adipogenesis. DEPTOR positively regulates adipogenesis by promoting the activity of the pro-adipogenic factors Akt/PKB and PPAR-gamma. These results establish DEPTOR as a physiological regulator of adipogenesis and provide new insights into the molecular mechanisms controlling WAT formation.
DEPTOR cell-autonomously promotes adipogenesis, and its expression is associated with obesity.
Sex, Specimen part
View SamplesWe used RNA sequencing to characterize gene expression of Ly75+/+ B1-8hi and Ly75-/- B1-8hi B cells from the germinal center light zone (LZ) 12 h after forcing positive selection of the Ly75+/+ population with anti-DEC205-OVA. Overall design: We primed C57BL/6 hosts with OVA-alum i.p. and after 2 weeks we adoptively transferred a mixture of B1-8hi B cells in which 15% were Ly75+/+ CD45.1 (DECP) and 85% were Ly75-/- CD45.1/2 (DECN). We then immunized the animals with NP-OVA in the footpads and after 6 days we injected anti-DEC205-OVA. 12 h or 24 h after anti-DEC205-OVA injection we sorted B220+ CD38- CD95+ CD45.1+ CD45.2- CD83hi CXCR4lo (DECPLZ) and B220+ CD38- CD95+ CD45.1+ CD45.2+ CD83hi CXCR4lo (DECNLZ) cells for whole transcriptome analysis by mRNA sequencing.
Germinal Center Selection and Affinity Maturation Require Dynamic Regulation of mTORC1 Kinase.
Specimen part, Cell line, Subject
View SamplesBackground and aims: The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers.
Stat3 is a negative regulator of intestinal tumor progression in Apc(Min) mice.
Sex, Specimen part
View SamplesThis experiment was designed to study oncogene-induced senescence (OIS). To this end we generated a series of cell lines derived from normal human diploid fibroblasts IMR90 forced to express the catalytic subunit of telomerase (hTERT). This cells were then subjected to further manipulation by orderly introducing defined genetic elements by retroviral transduction. The first cell line generated was ITV, which was obtained from the original cell line (IMR90 with hTERT) after introducing an empty vector. Subsequently, we introduced Mek:ER, which is a switchable version of the Mek kinase, a relevant downstream effector of Ras signaling during Ras-induced senescence, to generate ITM cells. We further modified this cell line by introducing SV40 small-t antigen (ST), papillomavirus oncoproteins E6 and E7 (E6/E7) or the combination of both (E6/E7 and ST). In this manner, we obtained ITMST, ITME6E7 and ITME6E7ST respectively.
Tumour biology: senescence in premalignant tumours.
No sample metadata fields
View SamplesWe have previously shown that total estrogen receptor alpha (ERalpha knockout (KO) mice exhibit hepatic insulin resistance. To investigate the contribution of hepatic ERalpha action for the observed phenotype, we established a liver-selective ERalphaKO mouse model, LERKO. We demonstrate that LERKO mice have efficient reduction of ERalpha selectively within the liver. However, LERKO and wild type control mice do not differ in body weight, and have a comparable hormone profile as well as insulin and glucose response, even when challenged with a high fat diet. Furthermore, LERKO mice display very minor changes in their hepatic transcript profile. Collectively, our findings indicate that hepatic ERalpha action may not be the initiating factor for the previously identified hepatic insulin resistance in ERalphaKO mice.
Estrogen signalling and the metabolic syndrome: targeting the hepatic estrogen receptor alpha action.
Sex, Specimen part
View SamplesBackground and aims: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6 type cytokine signaling required for hepatocyte proliferation and hepatoprotection but its role in sclerosing cholangitis (SC) and other cholestatic liver diseases remains unresolved. Methods: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2-/-) as a model for SC. Results: We demonstrate that conditional inactivation of stat3 in hepatocytes and cholangiocytes (stat3hc) of mdr2-/- mice strongly aggravated bile acid-induced liver injury and fibrosis. Similarly, stat3hc mice are more sensitive to cholic acid feeding than control mice. Global gene expression analysis demonstrated that hepatoprotective signals via epidermal growth factor and insulin-like growth factor 1 are affected upon loss of Stat3. Conclusions: Our data suggest that Stat3 protects cholangiocytes and hepatocytes from bile acid-induced damage thereby preventing liver fibrosis in cholestatic diseases.
Signal transducer and activator of transcription 3 protects from liver injury and fibrosis in a mouse model of sclerosing cholangitis.
Age, Specimen part
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