Arabidopsis thaliana wild type mechanical damage (MD) vs herbivore wounding (HW)
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ABSTRACT: Transcriptional profiling of Arabidopsis thaliana wild type (WT) comparing MD (mechanical damage) and HW (herbivore wounding). The differences in the biochemical responses to herbivory seen prompted us to search for less obvious differences between treatments using gene expression profiling. Biological replicates: 4 Two-condition experiment, MD vs. HW Arabidopsis leaves of WT plants. Biological replicates: 4 biological replicates.
Project description:This SuperSeries is composed of the following subset Series: GSE40922: Arabidopsis thaliana wild type control (C) vs Pseudomonas syringae infected (Pseu) GSE40923: Arabidopsis thaliana wild type mechanical damage (MD) vs herbivore wounding (HW) GSE40924: Arabidopsis thaliana wild type mechanical damage (MD) vs Myzus persicae wounding (Myz) Refer to individual Series
Project description:Transcriptional profiling of Arabidopsis thaliana wild type (WT) comparing MD (mechanical damage) and HW (herbivore wounding). The differences in the biochemical responses to herbivory seen prompted us to search for less obvious differences between treatments using gene expression profiling. Biological replicates: 4
Project description:Transcriptional profiling of Arabidopsis thaliana wild type (WT) and a line mutated in genes encoding plasmodesmata (PD) proteins (PDKO3) comparing MD (mechanical damage) and HW (herbivore wounding). The differences in the biochemical responses to herbivory seen in the PDKO3 when compared to the WT line, together with the absence of growth/developmental phenotypes in the former, prompted us to search for less obvious differences between the lines using gene expression profiling.
Project description:Transcriptional profiling of Arabidopsis thaliana wild type (WT) comparing mechanical damage (MD) and Myzus persicae feeding (Myz). The differences in the biochemical responses to insect feeding seen when compared to the control sample prompted us to search for less obvious differences between the treatments using gene expression profiling. Biological replicates: 4 biological replicates Two-condition experiment, MD vs. Myz Arabidopsis leaves of WT plants. Biological replicates: 4 biological replicates.
Project description:There is currently little information on which trancription factors control the expression of defence genes in response to herbivory in Arabidopsis thaliana. We performed a whole-genome analysis of Arabidopsis plants after feeding by Spodoptera littoralis larvae. Wild-type and knockout mutants in different insect-inducible transcription factors were either untreated (control plants) or challenged for 8 days with S. littoralis larvae (insect challenged plants).
Project description:To evaluate the differential potential affected by SMARCE1 -MD/MD(R42A) , we performed RNA-sequencing (RNA-seq) of Smarce1-MD and control Smarce1-MD (R42A) embrynoic body.
Project description:Transcriptional profiling of cotton fiber cells from two cotton germplasm lines, MD 52ne and MD 90ne. Comparison of fiber cell transcription profiles is between the two germplasm lines and over a developmental time-course from 8 to 24 days post anthesis in four day intervals.
Project description:To evaluate the effects of mitotic degradation of SMARCE1 upon gene expression, we performed RNA-sequencing (RNA-seq) of cultures of four independent subclones each of Smarce1-MD and control Smarce1-MD (R42A) mESCs. We found that transcription of the core pluripotency regulatory network was not disrupted. In contrast, GO analysis showed that neural differentiation-associated terms were enriched among genes upregulated in Smarce1-MD mESCs. To better understand the difference in neural fates in the neural induction experiments, we performed differential gene expression analysis and gene set enrichment analysis (GSEA) studies. Mitotic degradation of SMARCE1 resulted in higher expression of GABA receptors and hyper-activation of synaptic signaling on neural induction, indicating the aberrant neural cell fate commitment compared to SMARCE1-MD (R42A) cultures. And then we add back BMP4 to partically rescue the phenotype and very small amount of BMP4 will rescue the phenotype.
Project description:Lipid A (a hexaacylated 1,4 bis-phosphate) is a potent immune stimulant for TLR4/MD-2. Upon lipid A ligation, the TLR4/MD-2 complex dimerizes and initiates signal transduction. Historically, studies also suggested the existence of TLR4/MD-2-independent LPS signaling. Here we define the role of TLR4 and MD-2 in LPS signaling by using genome wide expression profiling in TLR4- and MD-2-deficient macrophages after stimulations with peptidoglycan-free LPS and synthetic E.coli lipid A. Of the 1,396 genes found significantly induced or repressed by any one of the treatments in the wildtype macrophages, none was present in the TLR4- or MD-2-deficient macrophages, confirming that the TLR4/MD-2 complex is the only receptor for endotoxin, and are both absolutely required for responses to LPS. Using a molecular genetics approach, we investigated the mechanism of TLR4/MD-2 activation by combining the known crystal structure of TLR4/MD-2 with computer modeling. We used lipid IVa, a defined lipid A mimetic to model the activation of mouse TLR4/MD2. The two phosphates on lipid A were predicted to interact extensively with the two positively charged patches mouse TLR4 according to our dimeric murine TLR4/MD-2/lipid IVa model. These two patches are composed of K263, R337, and K360 (Positive Patch 1), and K367 and R434 (Positive Patch 2). When either Positive Patch was abolished by mutagenesis into Ala, the responses to LPS and lipid A were almost abrogated. Thus, ionic interactions between the two phosphates on lipid A and the two positively charged patches on murine TLR4 appear to be essential for LPS receptor activation. The gene expression profile of macrophages from C57BL/6 and MD-2-deficient mice following either 10 ng LPS /mL, 100 ng lipid A/mL or 10 nM Pam2 stimulation for 2 hours were compared to PBS-stimulated control cells . In vitro differentiated macrophages from two individual WT and MD-2-deficient mice were cultured and stimulated with agonists separately, comparing the gene expression to PBS-stimulated control cells from the same mouse. Comparisons of PBS-stimulated WT cells to PBS-stimulated MD-2-deficient cells were performed to directly compare basal gene expression in the two genotypes.