Project description:Here we describe TROL (thylakoid rhodanese-like protein), a nuclear-encoded component of thylakoid membranes that is required for sustaining efficient linear electron flow in vascular plants. Thus, TROL might represent a missing thylakoid membrane linker for the assembly of a ternary complex between FNR, ferredoxin and NADP+. Such a complex is necessary for maintaining photosynthetic redox poise and balancing between several alternative electron-transport pathways of oxygenic photosynthesis. TROL inactivation modulates the expression of 638 nuclear genes, revealing a novel retrograde signaling pathway. Chloroplasts are the major source of NADPH which is exported to the cytosol where it participates in various redox-dependent processes. TROL is most likely the first element in a metabolic signaling pathway which influences the expression of a large set of stress related genes. Among them are O-methyltransferases and anthocyanin 5-aromatic acyltransferase which are highly upregulated. Microarray analysis was performed in order to identify metabolic networks and pathways regulated by the deficient protein TROL. Comparing ATH1 Affymetrix data results, 317 genes were down-regulated and 321 genes were classified as up-regulated, amongst which mostly affected enzymes were catalyses, oxigenases, monooxygenases and reductases involved in the process of photosynthesis.
Project description:Changes in tissue homeostasis, acquisition of invasive cell characteristics and tumor formation can often be linked to the loss of epithelial cell polarity. In carcinogenesis, the grade of neoplasia correlates with impaired cell polarity. In Drosophila, lgl, dlg and scribble, which are components of the epithelial apico-basal cell polarity machinery, act as tumor suppressors and orthologs of this evolutionary conserved pathway are lost in human carcinoma with high frequency. However, a mechanistic link between neoplasia and vertebrate orthologs of these tumor suppressor genes remains to be fully explored at the organismal level. Here, we show that the pen/lgl2 mutant phenotype shares two key cellular and molecular features of mammalian malignancy: cell autonomous epidermal neoplasia and epithelial-to-mesenchymal-transition (EMT) of basal epidermal cells including the differential expression of several regulators of EMT. Further we found that epidermal neoplasia and EMT in pen/lgl2 mutant epidermal cells is promoted by ErbB signalling, a pathway of high significance in human carcinomas. Intriguingly, EMT in the pen/lgl2 mutant is facilitated specifically by ErbB2 mediated E-cadherin mislocalization and not via canonical snail dependent down-regulation of E-cadherin expression. Our data reveal that pen/lgl2 functions as a tumor suppressor gene in vertebrates, establishing zebrafish pen/lgl2 mutants as a valuable cancer model.
Project description:Reference experiment of wild type Saccharomyces cerevisiae cells of the BJ5457 background. Cells were grown in synthetic complete medium (SC) with the addition of the necessary aminoacids and factors (leucine, uracil, histidine, tryptophane) and harvested in exponential phase (OD=0.7-1). Cells were grown in the presence of BCS and BPS chelators. <br>
Project description:1. Comparison of transcripts during growth in pure culture of a wild-type strain compared to a mutant deficient in the transcriptional activator encoded by the gene prhG.<br><br>2. Transcriptome analysis for identification of the prhG regulon by comparison of a prhG overexpressing mutant to the wild type strain.