Project description:In order to investigate the chicken SLCO1B3 gene functin on the liver metabolism, we used the Yimeng blue eggshell and brown eggshell chickens as the chicken liver SLCO1B3 gene knock-down animal to do the proteomic analysis.
Project description:Purpose:In order to assess the toxicity of AFB1 in chicken liver and the mechanism of curcumin alleviating AFB1-induced liver toxicity in chicken, we established a co-administered model to investigate LncRNA and mRNA profiles of chicken liver. Methods: RNA extracted by Total RNA Extractor (Trizol) was utilized to construct the final library. Libraries were pooled and sequenced on a 150-bp paired-end Illumina HiSeq™ 2000 run. The sequencing data obtained from Illumina Hiseq™ was filtered to get clean reads using Trimmomatic. The reads themselves and their matching reads which length was less than 35nt were removed. Clean reads were aligned to the reference sequence (Gallus_gallus-5.0, NCBI) using HISAT2. Results: Sampling directly from the liver yielded sufficient quantities of RNA to assess transcripts from each chicken and mapped to 24,883 Gallus gallus genes. Conclusions: We used the method of RNA-seq to find the target genes and related signaling pathways involved in the co-administered (AFB1 and curcumin) and their underlying mechanisms.
Project description:We show that RORγ functions as a master activator of the entire mevalonate pathway-cholesterol biosynthesis program in the porcine liver. RORγ genome-wide binding enrichments in the liver were significantly reduced in response to mycotoxin exposure.
Project description:This dataset has been generated to identify promoter regions in the chicken genome to distinguish active and inactive genes. We focussed our analyses on actively transcribed tRNA and mRNAs genes. Chicken liver was cross-linked to capture histone-DNA interactions. Sequencing libraries were prepared from H3K4me3-precipitated DNA and input control.
Project description:Fungal secondary metabolites can not only cause toxic effects in animals and humans, but also serve as virulence factors of the producing fungi for causing plant diseases.Thus, the severity of plant diseases associated with mycotoxins depend on the sensitivity towards the toxin. In previous experiments, we have evaluated the phytotoxic effect ofa mycotoxin on root growth of Arabidopsis wild-type and mutant seedlings. Mycotoxin treatment of a new conditional root expansion mutant partially restores the expansion phenotype (JE100; Werner et al., unpublished). AIM: This experiment aims to identify genes, in early and later phases after mycotoxin treatment in wild-type and mutant seedlings. EXPERIMENTAL PLAN: Eight Affymetrix chips are needed for this experiment. RNA preparation will be provided from wild-type, accession Columbia, and mutant seedlings after different time points of mycotoxin treatment. As control, separate seedlings will be treated with the same concentration of solvent (DMSO). Briefly, seeds will be sterilized, stratified for 48 hours and germinated on MS agar plates containing 4.5% sucrose at 22°C and 16h/8h light/dark cycles. 10 days after germination, seedlings will be transferred to liquid MS medium and shaken for another 3 days for acclimatization. Seedlings will be harvested after 2 and 24 hours of treatment with a single concentration (50 µM) of mycotoxin. To account for experimental variations (i.e. time needed for freezing the tissues, circadian clock,...), the experiment will be repeated three times and RNA samples will be pooled. EXPECTED RESULTS: The experiment should identify genes differentially expressed: 1) between wild-type and mutant seedlings, 2) upon mycotoxin treatment in wild-type, 3) upon mycotoxin treatment of mutant seedlings and 4) upon solvent treatment. The results will allow us to pinpoint the mode of action of this mycotoxin. They will also allow us to better understand the function of the mutated gene which affects the sensitivity towards the mycotoxin. Furthermore, we expect to identify the signaling pathway by which the plant responses towards the mycotoxinis triggered. Experimenter name = Ulrike Werner Experimenter phone = +43-1-36006-6371 Experimenter fax = +43-1-36006-6392 Experimenter department = Institute of Applied Genetics and Cell Biology Experimenter institute = BOKU Experimenter address = Center of Applied Genetics Experimenter address = University of Agricultural Sciences Vienna Experimenter address = Muthgasse 18 Experimenter address = Vienna Experimenter zip/postal_code = 1190 Experimenter country = Austria Keywords: genetic_modification_design; compound_treatment_design; time_series_design
Project description:The mycotoxin deoxynivalenol (DON) is a secondary metabolite from Fusarium species and is frequently present on wheat and other cereals. The main effects of DON are a reduction of the feed intake and reduced weight gain of broilers. At the molecular level DON binds to the 60S ribosomal subunit and inhibits subsequently protein synthesis at the translational level. It has been suggested that cells and tissues with high protein turnover rate, like the liver and small intestine, are most affected by DON. However, little is known about other effects of DON e.g. at the transcriptional level. Therefore we decided to perform a microarray analysis, which allows us the investigation of thousands of transcripts in one experiment. The one-day old broiler chicks were separated into four groups. The diets consisted of a control diet and of three diets with moderate concentrations of 1.0, 2.5 and 5.0 mg DON/kg feed, which was attained by exchanging uncontaminated wheat with naturally DON-contaminated wheat up to the intended concentration. The chicken were held at standard conditions for 23 days and received their diet ad libitum. After slaughter the gene expression was determined in the liver of three samples per group.