Project description:Unlike pathogens that trigger plant defense responses, beneficial microbes are compatible with plants. One possible reason for the compatibility is that the microbial factors from beneficial microbes are inert in that they do not trigger plant defense responses. Little is known about the mechanisms underlying this seemingly inert relation. Here we report that Arabidopsis lacking the gene Growth-Promotion 1 (GP1) becomes defensive to microbial volatiles from Bacillus amyloliqueficiens strain GB03, a beneficial rhizobacterium. The gp1 mutant was isolated in a forward genetic screen for mutants that show defectiveness in GB03-triggered plant inducible vigor. GP1 encodes a stearoyl-ACP desaturase that catalyzes the desaturation of stearic acid (18:0) to oleic acid (18:1). Consistently, plant inducible vigor was also impaired by chemical enhancement of 18:1 catabolism, while genetic disruption of 18:1 catabolism largely restored the inducible vigor in gp1. When exposed to GB03-emitted microbial volatiles (GMVs), wild type plants showed transcriptional up-regulation of growth-promoting processes and down-regulation of defense responses; in contrast, the gp1 transcriptome displayed elevated defense responses when treated with GMVs. Meanwhile disruption of salicylic acid-mediated defense partially restored plant inducible vigor in gp1. Microbiota profiling revealed that GP1 dysfunction alters the assemblage of plant-associated rhizobacteria communities, including a reduction in the Bacillaceae family that is known to contain many beneficial rhizobacteria species. Consistently, gp1 mutants showed severely impaired root colonization of GB03. Our findings suggest that GP1 prevents the plant defense system from being mistakenly activated by non-pathogenic microbial factors, thereby allowing mutualistic association between the plant and beneficial microbes.
Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.
Project description:⢠Selected soil-borne rhizobacteria can trigger an induced systemic resistance (ISR) that is effective against a broad spectrum of pathogens. In Arabidopsis thaliana, the root-specific transcription factor MYB72 is required for the onset of ISR, but is also associated with plant survival under conditions of iron deficiency. Here we investigated the role of MYB72 in both processes. ⢠To identify MYB72 target genes, we analyzed the root transcriptomes of wild-type Col-0, mutant myb72, and complemented 35S:FLAG-MYB72/myb72 plants in response to ISR-inducing Pseudomonas fluorescens WCS417. ⢠Five WCS417-inducible genes were misregulated in myb72 and complemented in 35S:FLAG-MYB72/myb72. Amongst these, we uncovered β-glucosidase BGLU42 as a novel component of the ISR signaling pathway. Overexpression of BGLU42 resulted in constitutive disease resistance, whereas bglu42 was defective in ISR. Furthermore, we found 195 genes to be constitutively upregulated in MYB72-overexpressing roots in the absence of WCS417. Many of these encode enzymes involved in the production of iron-mobilizing phenolic metabolites under conditions of iron deficiency. We provide evidence that BGLU42 is required for their release into the rhizosphere. ⢠Together, this work highlights a thus far unidentified link between the ability of beneficial rhizobacteria to stimulate systemic immunity and mechanisms induced by iron deficiency in host plants. Total 18 samples of RNA extracted from Arabidopsis roots: Three genotypes: 1) Wild-type Arabidopsis thaliana accession Col-0, 2) mutant myb72-2 (Col-0 background), 3) Transgenic 35S:FLAG-MYB72 (oxMYB72) in the myb72-2 background; Two treatments: 1) non-treated control, 2) Roots colonized by beneficial Pseudomonas fluorescens WCS417 rhizobacteria; Replicates: three biological replicates per genotype/treatment combination
Project description:Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. We found that SCD1 inhibition alters the levels of proteins phosphorylated at tyrosine in fibroblasts. Major regulated proteins were identified following immunoprecipitation using an anti-phospho-tyrosine antibody and subsequent proteomic analysis.
Project description:Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes. We used microarrays to examine gene expression in differentiated pre-adipocytes treated with and without an SCD inhibitor.
Project description:Volatiles of certain rhizobacteria can cause growth inhibitory effects on plants/ Arabidopsis thaliana. How these effects are initiated and which mechanisms are enrolled is not yet understood. Obviously the plant can survive/live with the bacteria in the soil, which suggest the existance of a regulatory mechanism/network that provide the possibility for coexistance with the bacteria. To shed light on this regulatory mechanism/network we performed a microarray anlaysis of Arabidopsis thaliana co-cultivated with two different rhizobacteria strains. In this study we used the ATH1 GeneChip microarray to investigate the transcriptional response of 4 to 5 days old Arabidopsis thaliana seedlings at 6 h, 12 h and 24 h exposure to volatiles of the rhizobacteria Serratia plymuthica HRO-C48 or Stenotrophomonas maltophilia R3089.