Dynamic histone modifications establish the two phase kinetics of glucosinolates against wounding stress in Arabidopsis plant
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE239725 | GEO | 2024/01/31
REPOSITORIES: GEO
Similar Datasets
Project description:Sulfur-deficiency-induced repressor proteins optimize glucosinolate biosynthesis in plants Glucosinolates (GSLs) in the plant order of the Brassicales are sulfur-rich secondary metabolites harboring anti-pathogenic and anti-herbivory plant-protective functions as well as possessing medicinal properties such as carcinopreventive and antibiotic activities. Plants repress GSL biosynthesis upon sulfur deficiency (–S), hence, field performance and medicinal quality are impaired by inadequate sulfate supply. The molecular mechanism linking –S to GSL biosynthesis has remained understudied. We report here the identification of the –S marker genes Sulfur deficiency induced1 and Sulfur deficiency induced2 (SDI1, SDI2) acting as major repressors controlling GSL biosynthesis in Arabidopsis under –S condition. SDI1 and SDI2 expression negatively correlated with GSL biosynthesis in both transcript and metabolite levels. Principal component analysis of transcriptome data indicated that SDI1 regulates aliphatic GSL biosynthesis as part of –S-response. SDI1 was localized to the nucleus and interacted with MYB28, a major transcription factor promoting aliphatic GSL biosynthesis, in both yeast and plant cells. SDI1 inhibited transcription of aliphatic GSL biosynthetic genes through maintaining the DNA-binding composition in a form of a SDI1-MYB28 complex, leading to down-regulate GSL biosynthesis and prioritize sulfate usage for primary metabolites under sulfur-deprived conditions.
2016-10-07 | GSE81347 | GEO
Project description:In this study, we found that a light signaling factor, Long Hypocotyl 5 (HY5) is closely involved in the regulation of GSLs contents in light condition. In addition, HY5 was shown to physically interact with a histone deacetylase HDA9 and bind to proximal promoter region of MYB29 and IMD1 to suppress aliphatic GSL biosynthetic process. These results demonstrate that HY5 acts to suppress GSL accumulation at daytime, thus properly modulating the GSL contents on a daily basis of Arabidopsis plant.
2024-06-12 | GSE250418 | GEO
Project description:Dynamic histone modifications establish the two phase kinetics of glucosinolates against wounding stress in Arabidopsis plant
| PRJNA1000626 | ENA
Project description:We analyzed transcriptome changes from germinating cyp79B2 cyp79B3, qko, and pad3 mutant Arabidopsis seeds. Here were used mutant lines in Col-0 genetic background: a cyp79B2 cyp79B3 double mutant defective in indolic glucosinolate (cyp79B2/B3), a cyp79B2 cyp79B3 myb28 myb29 quadruple mutant defective in indolic and aliphatic glucosinolates (qko), and a camalexin deficient mutant (pad3). Differentially expressed genes were identified at 3, 6 and 10 days after sowing from both the mutant line seeds and from Alternaria brassicicola when inoculated seeds were analyzed.
2024-03-26 | GSE214602 | GEO
Project description:Recent studies have reported that glycosphingolipids (GSL) might be involved in obesity induced insulin resistance. Those reports suggested that inhibition of GSL biosynthesis in animals ameliorated insulin sensitivity accompanied with improved glycemic control leading to decreased liver steatosis in obese mice. In addition, GSL depletion altered hepatic secretory function. In those studies, ubiquitously acting inhibitors for GSL-biosynthesis have been used to inhibit function of the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide based GSL-synthesis pathway. In the present study, a genetic approach for GSL deletion in hepatocytes was chosen to achieve full inhibition of GSL synthesis and to prevent possible adverse effects caused by Ugcg-inhibitors. Using the Cre/loxP system under control of the albumin promoter, GSL biosynthesis in hepatocytes and their release into the plasma could be effectively blocked. Deletion of GSL in hepatocytes did not change quantity of bile excretion through the biliary duct. Total bile salt content in bile-, feces- and plasma from mutant mice showed no difference as compared to control animals. Cholesterol concentration in liver-, bile-, feces- and plasma-samples remained unaffected. Lipoprotein concentration in plasma-samples in mutant animals reached similar levels as in their control littermates. No alteration in glucose tolerance after intraperitoneal application of glucose and insulin appeared in mutant animals. A preventive effect of GSL-deficiency on development of liver steatosis after high fat diet feeding could not be observed. Conclusion: The data suggest that GSL in hepatocytes are not essential for sterol, glucose and lipoprotein metabolism and do not prevent high fat diet-induced liver steatosis, indicating that Ugcg inhibitors exert their effect on hepatocytes either independently of GSL or mediated by other (liver) cell types. Comparison of wildtype mouse liver function versus Ugcg-deficient
2010-05-14 | E-GEOD-19316 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to analyze the transcriptome of Arabidopsis thaliana treated after flg22 and to find changes of glucosinolate metabolism genes after treatment. Methods: Total mRNA of 10 day wild-type Arabidopsis seedlings that were treated with and without flg22( final concentrations 1μmol/L) in 1/2 MS medium for 4h, were extracted respectively. Each sample was harvested in three independent biological replicates with equal weight and mixed ,subsequently sequencing. The sequence reads that passed quality filters were mapped to the Arabidopsis_thaliana genome (TAIR10.18).Then the mapping genes were used for the abundance and functional analysis. Results: We mapped about 45 million and 52 million sequence reads of control sample and treatment sample to the Arabidopsis_thaliana genome (TAIR10.18) and identified total 23,413 genes with Botiw/TopHat workflow. Comparison of the two samples showed 1,200 differentially expressed genes (DEGs), including 290 down-regulated and 910 up-regulated genes. The DEGs were associated with energy metabolism, amino acid metabolism and biosynthesis of secondary metabolites. After flg22 treatment, genes involved in indolic glucosinolate biosynthesis pathway were up-regulated significantly，which is further demonstrated by Real Time RT-PCR, while aliphatic glucosinolate pathway almost had no change, indicating the important role of indolic glucosinolates in plant defense responses. Conclusion: Our study provides the overall genetic resource of Arabidopsis_thaliana after treated by flg22 to date. These data will pave the way for further studies about deeply understand pathogen induced defense and the contribution of indolic glucosinolates.
2017-03-22 | GSE56117 | GEO
Project description:Recent studies have reported that glycosphingolipids (GSL) might be involved in obesity induced insulin resistance. Those reports suggested that inhibition of GSL biosynthesis in animals ameliorated insulin sensitivity accompanied with improved glycemic control leading to decreased liver steatosis in obese mice. In addition, GSL depletion altered hepatic secretory function. In those studies, ubiquitously acting inhibitors for GSL-biosynthesis have been used to inhibit function of the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide based GSL-synthesis pathway. In the present study, a genetic approach for GSL deletion in hepatocytes was chosen to achieve full inhibition of GSL synthesis and to prevent possible adverse effects caused by Ugcg-inhibitors. Using the Cre/loxP system under control of the albumin promoter, GSL biosynthesis in hepatocytes and their release into the plasma could be effectively blocked. Deletion of GSL in hepatocytes did not change quantity of bile excretion through the biliary duct. Total bile salt content in bile-, feces- and plasma from mutant mice showed no difference as compared to control animals. Cholesterol concentration in liver-, bile-, feces- and plasma-samples remained unaffected. Lipoprotein concentration in plasma-samples in mutant animals reached similar levels as in their control littermates. No alteration in glucose tolerance after intraperitoneal application of glucose and insulin appeared in mutant animals. A preventive effect of GSL-deficiency on development of liver steatosis after high fat diet feeding could not be observed. Conclusion: The data suggest that GSL in hepatocytes are not essential for sterol, glucose and lipoprotein metabolism and do not prevent high fat diet-induced liver steatosis, indicating that Ugcg inhibitors exert their effect on hepatocytes either independently of GSL or mediated by other (liver) cell types.
2010-02-04 | GSE19316 | GEO
Project description:Mechanical wounding of Arabidopsis thaliana leaves results in modifications of most membrane lipids within 6 hours. Here, we discuss the lipid changes, their underlying biochemistry, and possible relationships among activated pathways. New evidence is presented supporting the role of the processive galactosylating enzyme SENSITIVE TO FREEZING2 in the wounding response.
| S-EPMC4883853 | biostudies-literature
Project description:Plants respond to wounding stress by changing gene expression patterns and inducing the production of hormones including jasmonic acid. This wounding transcriptional response activates specialized metabolism pathways such as the glucosinolate pathways in Arabidopsis thaliana. While the regulatory factors and sequences controlling a subset of wound-response genes are known, it remains unclear how wound response is regulated globally. Here, we how these responses are regulated by incorporating putative cis-regulatory elements, known transcription factor binding sites, in vitro DNA affinity purification sequencing, and DNase I hypersensitive sites to predict genes with different wound-response patterns using machine learning. We observed that regulatory sites and regions of open chromatin differed between genes upregulated at early and late wounding time-points as well as between genes induced by jasmonic acid and those not induced. Expanding on what we currently know, we identified cis-elements that improved model predictions of expression clusters over known binding sites. Using a combination of genome editing, in vitro DNA-binding assays, and transient expression assays using native and mutated cis-regulatory elements, we experimentally validated four of the predicted elements, three of which were not previously known to function in wound-response regulation. Our study provides a global model predictive of wound response and identifies new regulatory sequences important for wounding without requiring prior knowledge of the transcriptional regulators.
| S-EPMC8824630 | biostudies-literature