Project description:Microcystin-LR (MC-LR) is a potent hepatotoxin for which a substantial gap in knowledge persists regarding the underlying molecular mechanisms of liver toxicity and injury. Although long non-coding RNAs (lncRNAs) have been extensively studied in model organisms, our knowledge concerning the role of lncRNAs in liver injury is limited. Given that lncRNAs show low levels of sequence conservation, their role becomes even more unclear in non-model organisms without an annotated genome, like whitefish (Coregonus lavaretus). The objective of this study was to discover and profile aberrantly expressed polyadenylated lncRNAs that are involved in MC-LR-induced liver injury in whitefish. Using RNA sequencing (RNA-Seq) data, we de novo assembled a high-quality whitefish liver transcriptome. This enabled us to find 94 differentially expressed (DE) putative evolutionary conserved lncRNAs, such as MALAT1, HOTTIP, HOTAIR or HULC, and 4429 DE putative novel whitefish lncRNAs, which differed from annotated protein-coding transcripts (PCTs) in terms of minimum free energy, guanine-cytosine (GC) base-pair content and length. Additionally, we identified DE non-coding transcripts that might be 3′ autonomous untranslated regions (3′UTRs) of mRNAs. We found both evolutionary conserved lncRNAs as well as novel whitefish lncRNAs that could serve as biomarkers of liver injury.
Project description:Stress represents a major factor negatively affecting fish welfare in aquaculture. The objective of the present study was to identify and evaluate informative indicators for the welfare of maraena whitefish (Coregonus maraena) exposed to inconvenient temperatures. The present study compares the physiological impact of either acute or gradual temperature rise from 18 °C to 24 °C on maraena whitefish in aquaculture. We analysed microarray-based transcriptome profiles in liver, spleen and kidney and identified a common set of diagnostic biomarkers each indicating thermal stress induced by acute or gradual temperature rise in the selected tissues. We identified common and unique tissue- and stress mode-specific pathways reflecting metabolic, cell signalling and immunologic crossroads to cope with thermal stress.
