Project description:We used RNAseq to quantify trascript expression from three populations of Conyza sumatrensis before and 5 hours after treatment with 2,4-D. This study investigates different responses between a 2,4-D resistant biotype compared to a 2,4-D sensitive biotype.
Project description:Nontarget-site resistance due to rapid physiological response in 2,4-D resistant Conyza sumatrensis: Reduced 2,4-D translocation and auxin-induced gene expression
Project description:Resistance to the phenoxy synthetic auxin herbicide 2,4-D is conferred by a deletion mutation in the degron tail of IAA2. An RNA-Seq experiment was used to assemble a reference transcriptome for the weed species Sisymbrium orientale, to quantify gene expression, and to identify sequence variants in the alignments. A 27 bp deletion was identified in the IAA2 gene. Forward genetics supported the role of this deletion mutation in resistance. The IAA2 deletion allele was transformed into Arabidopsis thaliana to confirm that it conferred 2,4-D resistance.
Project description:To identify intrinsic mechanismis that mediating Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance , gene expression analysis was performed on MDA-MB-231 cell lines exposed to TRAIL, in parental (Sensitive) or treat to resistance (TTR) conditions.
Project description:The regulation of necrotic death and its relevance in anti-cancer therapy are largely unknown. Here we have investigated the pro-apoptotic and pro-necrotic activities of two ubiquitin-proteasome system inhibitors (UPSIs): bortezomib and G5. The present study points out that the glioblastoma cell lines U87MG and T98G are useful models to study the susceptibility to apoptosis and necrosis in response to UPSIs. U87MG cells are resistant to apoptosis induced by bortezomib and G5 but susceptible to necrosis induced by G5. On the opposite T98G cells are susceptible to apoptosis induced by both inhibitors but show some resistance to G5-induced necrosis. By comparing the transcriptional profiles of the two cell lines, we have found that the resistance to G5-induced necrosis could arise from differences in glutathione synthesis/utilization and in the microenvironment. In particular collagen IV, which is highly expressed in T98G cells, and fibronectin, whose adhesive function is counteracted by tenascin-C in U87MG cells, can restrain the necrotic response to G5. Collectively, our results provide an initial characterization of the molecular signals governing cell death by necrosis in glioblastoma cell lines. Experiment Overall Design: Gene expression profiling was evaluated from 3 replicates each of T98G and U87MG cells.
