Jomthonic acids biosynthesis gene cluster
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB25588 | ENA |
REPOSITORIES: ENA
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Project description:In response to biotic stress, plants produce suites of highly modified fatty acids that bear unusual chemical functionality. Despite their chemical complexity and proposed roles in pathogen defense, little is known about the biosynthesis of these decorated fatty acids in plants. Falcarindiol is a prototypical acetylenic lipid present in carrot, tomato, and celery that inhibits growth of fungi and human cancer cell lines. Using a combination of untargeted metabolomics and RNA sequencing, we discovered a biosynthetic gene cluster in tomato (Solanum lycopersicum) that is required for the production of falcarindiol in response to an adapted fungal pathogen, Cladosporium fulvum. By reconstituting the initial biosynthetic steps in a heterologous host (Nicotiana benthamiana) and generating transgenic pathway mutants in tomato, we demonstrate a direct role for three genes in the cluster in falcarindiol biosynthesis. This work reveals a mechanism by which plants sculpt their lipid pool in response to pathogens, and provides critical insight into the complex biochemistry of alkynyl lipid production.
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Project description:Macrophage-mediated inflammation is a major contributor to obesity-associated insulin resistance. The corepressor NCoR interacts with inflammatory pathway genes in macrophages, suggesting that its removal would result in increased activity of inflammatory responses. Surprisingly, we find that macrophage-specific deletion of NCoR instead results in an anti-inflammatory phenotype along with robust systemic insulin sensitization in obese mice. We present evidence that de-repression of LXRs contributes to this paradoxical anti-inflammatory phenotype by causing increased expression of genes that direct biosynthesis of palmitoleic acid and M-OM-^I3 fatty acids. Remarkably, the increased M-OM-^I3 fatty acid levels primarily inhibit NF-M-NM-:B-dependent inflammatory responses by uncoupling NF-M-NM-:B binding and enhancer/promoter histone acetylation from subsequent steps required for pro-inflammatory gene activation. This provides a mechanism for the in vivo anti-inflammatory insulin sensitive phenotype observed in mice with macrophage-specific deletion of NCoR. Therapeutic methods to harness this mechanism could lead to a new approach to insulin sensitizing therapies. ChIP-Seq and Gro-Seq profiling was performed in thioglycollate-elicited peritoneal macrophages treated as indicated.
2013-10-09 | E-GEOD-50944 | biostudies-arrayexpress
Project description:Macrophage-mediated inflammation is a major contributor to obesity-associated insulin resistance. The corepressor NCoR interacts with inflammatory pathway genes in macrophages, suggesting that its removal would result in increased activity of inflammatory responses. Surprisingly, we find that macrophage-specific deletion of NCoR instead results in an anti-inflammatory phenotype along with robust systemic insulin sensitization in obese mice. We present evidence that de-repression of LXRs contributes to this paradoxical anti-inflammatory phenotype by causing increased expression of genes that direct biosynthesis of palmitoleic acid and ω3 fatty acids. Remarkably, the increased ω3 fatty acid levels primarily inhibit NF-κB-dependent inflammatory responses by uncoupling NF-κB binding and enhancer/promoter histone acetylation from subsequent steps required for pro-inflammatory gene activation. This provides a mechanism for the in vivo anti-inflammatory insulin sensitive phenotype observed in mice with macrophage-specific deletion of NCoR. Therapeutic methods to harness this mechanism could lead to a new approach to insulin sensitizing therapies.
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Project description:Despite the importance of amino acids as basic components of proteins, amino acids also serve as substrates for multiple other metabolic pathways, such as the TCA cycle that regulates energy homeostasis. The response to deficiency in the biosynthesis of specific amino acids (also termed âamino acid starvationâ) has been studied extensively in yeast (See for example Petti et. al., 2011 Survival of starving yeast is correlated with oxidative stress response and non-respiratory mitochondria function. Proc. Natl. Acad. Sci. USA 108: 1089-1098). In contrast, very little is known about the metabolic responses to deficiency in the biosynthesis of amino acids in plants. A number of recent reports have already shown that catabolism of amino acids can significantly contribute to cellular energy homeostasis particularly during the nighttime and particularly in response to stress. In the present manuscript we used a previously characterized Arabidopsis mutant with reduced expression of the Lys biosynthesis enzyme L,L-diaminopimelate aminotransferase (dapat) to investigate the physiological and metabolic impacts of deficient Lys biosynthesis. The results obtained demonstrate that not stomatal limitations but rather biochemical alterations are responsible for the decreased photosynthesis and growth of the dapat mutants which mimic stress conditions associated to Lys deficiency. Our findings suggest that manipulation of Lys biosynthesis in dapat mutant simulates a stress response culminating in a highly exquisite metabolic reprogramming such that alternative substrates support energy generation once carbohydrate metabolism is down-regulated.
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