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Root Transcriptome of WT, SDI1 Overexpression Lines and sdi1sdi2 Double Knockouts Grown under Sulfur Sufficient and Deficient Conditions

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE81347 | GEO | 2016/10/07

SECONDARY ACCESSION(S): PRJNA321336

REPOSITORIES: GEO

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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

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Root Transcriptome of WT, SDI1 Overexpression Lines and sdi1sdi2 Double Knockouts Grown under Sulfur Sufficient and Deficient Conditions

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