Project description:We report the application of a high-throughput technique, RNA-seq, to study the transcriptomic response of Bacillus subtilis growing in the presence of Botrytis cinerea. In addition, we study the transcriptomic response of Botrytis cinerea when cocultured with Bacillus subtilis and also the transcriptomic response of Botrytis treated with purified TasA and Fengycin after 6h
Project description:In this study, tomato plants were exogenously treated with either 20nM of he peptide systemin at 20nM or water by soil drenched. 24 hours after the treatment, tomato plants were challenged with the necrotrophic fungus Botrytis cinerea. We performed proteomic, metabolomic and enzymatic studies to decipher the Sys-induced changes in tomato plants either in the absence or the presence of Botrytis cinerea infection. Sys-treatments triggered direct proteomic rearrangement mostly involved in carbon metabolism and photosynthesis. However, the final induction of defence proteins required concurrent challenge, triggering priming of pathogen-targeted proteins. the proteomic analysis revealed that Sys conditioned the primary metabolism towards the production of available sugars that could be fuelling the priming of callose deposition in Sys-treated, furthermore PR1 revealed as key element in System,in-induced resistance.
Project description:First try at GNPS. Bacillus mycoides is being investigated as a potential biological control agent against Botrytis cinerea, and we wish to elucidate what compounds are causing the inhibition of Botrytis cinerea growth. Bacillus mycoides was cultured in NB, Botrytis cinerea was cultured in NB, then B. cinerea and B. mycoides were cultured in NB together.
Project description:Transcriptional profiling of Arabidopsis leaves comparing mock-treated leaves with Botrytis cinerea infected leaves over a time-course (12 and 24 hrs).
Project description:The intermediate filament protein Nestin serves as a biomarker for stem cells and has been used to identify subsets of cancer stem-like cells. However, the mechanistic contributions of Nestin to cancer pathogenesis are not understood. Here we report that Nestin binds the hedgehog pathway transcription factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype. In a mouse model system, Nestin levels increased progressively during medulloblastoma formation resulting in enhanced tumor growth. Conversely, loss of Nestin dramatically inhibited proliferation and promoted differentiation. Mechanistic investigations revealed that the tumor-promoting effects of Nestin were mediated by binding to Gli3, a zinc finger transcription factor that negatively regulates hedgehog signaling. Nestin binding to Gli3 blocked Gli3 phosphorylation and its subsequent proteolytic processing, thereby abrogating its ability to negatively regulate the hedgehog pathway. Our findings show how Nestin drives hedgehog pathway-driven cancers and uncover in Gli3 a therapeutic target to treat these malignancies. Nestin+ and Nestin- GNPs (granule neuron precursors) were purified from Nestin-CFP/Math1-Cre/Ptch1-loxp cerebella at postnatal day 4 by FACs, and total RNA from these two cell populations were extracted, and then labeled and hybridized to Affymetrix Mouse Genome 430 2.0 arrays.