EC Number   |
General Information |
Reference |
|---|
   2.4.1.173 | evolution |
enzyme UGT51 is a member of the GT1 family, GT-B fold group, comprising two Rossman-like domains |
-, 759680 |
| 2.4.1.173 | evolution |
phylogenetic tree of UGT80- and UGT713-related proteins, overview |
-, 736570 |
| 2.4.1.173 | evolution |
the enzyme belongs to the UDP-glucose sterol glycosyltransferases family of developmental and stress regulated genes that encode cytosolic and membrane-associated forms of the enzyme. Identification and functional characterization of the four members, SlSGT1-4, of the tomato cv. Micro-Tom |
759277 |
| 2.4.1.173 | evolution |
the enzyme is a member of SGT gene family |
723149 |
| 2.4.1.173 | evolution |
the genome of Arabidopsis thaliana contains two genes coding for UDP-Glc:sterol-glucosyltransferases, UGT80A2 and UGT80B1, and studies of mutant lines indicate that they are only partially redundant |
-, 760156 |
| 2.4.1.173 | evolution |
UGT80 proteins belong to a third family that is hypothesized to be involved in sterol glucoside synthesis, phylogenetic tree of UGT80- and UGT713-related proteins, overview |
-, 736570 |
| 2.4.1.173 | malfunction |
analysis of the function of SGTs by silencing SGTL1, SGTL2 and SGTL4 in Withania somnifera. Downregulation of SGTs by artificial miRNAs leads to the enhanced accumulation of withanolide A, withaferin A, sitosterol, stigmasterol and decreased content of withanoside V in virus induced gene silencing (VIGS) lines. This is further correlated with increased expression of WsHMGR, WsDXR, WsFPPS, WsCYP710A1, WsSTE1 and WsDWF5 genes, involved in withanolide biosynthesis. These variations of withanolide concentrations in silenced lines result in pathogen susceptibility as compared to control plants. The infection of Alternaria alternata causes increased salicylic acid, callose deposition, superoxide dismutase and H2O2 in aMIR-VIGS lines. The expression of biotic stress related genes, namely, WsPR1, WsDFS, WsSPI and WsPR10 is also enhanced in aMIR-VIGS lines in time dependent manner. Salicylic acid level increases the expression of defence related genes in silenced lines. A positive feedback regulation of withanolide biosynthesis occurs by silencing of SGTLs which results in reduced biotic tolerance |
760139 |
| 2.4.1.173 | malfunction |
inactivation of UDP-glucose sterol glucosyltransferases enhances Arabidopsis thaliana resistance to Botrytis cinerea infection, which correlates with increased levels of jasmonic acid (JA) and upregulation of two marker genes (PDF1.2 and PR4) of the ERF branch of the JA signaling pathway. Analysis of the response to necrotrophic fungus Botrytis cinerea in an Arabidopsis thaliana mutant that is severely impaired in steryl glycosides biosynthesis due to the inactivation of the two sterol glucosyltransferases, UGT80A2 and UGT80B1. The mutant also accumulates higher levels of camalexin, the major Arabidopsis thaliana phytoalexin, than wild-type plants. Camalexin accumulation correlates with enhanced transcript levels of several cytochrome P450 camalexin biosynthetic genes, as well as of their transcriptional regulators WRKY33, ANAC042, and MYB51, suggesting that the Botrytis-induced accumulation of camalexin is coordinately regulated at the transcriptional level. After fungus infection, the expression of genes involved in the indole glucosinolate biosynthesis is also upregulated at a higher degree in the ugt80A2;B1 mutant than in wild-type plants |
-, 759256 |
| 2.4.1.173 | malfunction |
the atg26 mutant is defective in Appressorium-mediated host invasion |
706211 |
| 2.4.1.173 | malfunction |
the plasma membrane cell fate regulator, SCRAMBLED (SCM), is mislocalized in ugt80B1 mutants, underscoring the aberrant root epidermal cell patterning. GFP-tagged SCM is localized to the cytoplasm in a non cell type dependent manner instead of the hair (H) cell plasma membrane in these mutants. Abnormal root hair cell patterning in ugt80B1 mutants is likely the direct result of expression of GL2 in H cell files in this mutant. The aberrant expression of GL2 is caused by the mislocalization of SCM away from the cell periphery, reducing the capacity of the receptor to mediate positional information to the cell. Reductions in specific sterol glucosides might be responsible for the disruption of cell fate regulators in these ugt80B1 mutants. The mislocalization of SCM to the cytoplasm can point to a role for sterol glucosides in vesicular trafficking or plasma membrane protein targeting. Deficiencies in specific sterol glucosides are sufficient to disrupt normal cell function and point to a possible role for sterol glucosides in cargo transport and/or protein targeting to the plasma membrane. Aberrant subcellular localization of SCM:GFP in ugt80B1 epidermal cells from the elongation zone of the root |
-, 760156 |
