Methyl Salicylate Glucosylation Regulates Plant Defense Signaling and Systemic Acquired Resistance.

Plant systemic acquired resistance (SAR) provides an efficient broad-spectrum immune response to pathogens. SAR involves mobile signal molecules that are generated by infected tissues and transported to systemic tissues. Methyl salicylate (MeSA), a molecule that can be converted to salicylic acid (SA), is an essential signal for establishing SAR, particularly under a short period of exposure to light after pathogen infection. Thus, the control of MeSA homeostasis is important for an optimal SAR response. Here, we characterized a uridine diphosphate-glycosyltransferase, UGT71C3, in Arabidopsis (Arabidopsis thaliana), which was induced mainly in leaf tissue by pathogens including Pst DC3000/avrRpt2 (Pseudomonas syringae pv tomato strain DC3000 expressing avrRpt2). Biochemical analysis indicated that UGT71C3 exhibited strong enzymatic activity toward MeSA to form MeSA glucosides in vitro and in vivo. After primary pathogen infection by Pst DC3000/avrRpt2, ugt71c3 knockout mutants exhibited more powerful systemic resistance to secondary pathogen infection than that of wild-type plants, whereas systemic resistance in UGT71C3 overexpression lines was compromised. In agreement, after primary infection of local leaves, ugt71c3 knockout mutants accumulated significantly more systemic MeSA and SA than that in wild-type plants. whereas UGT71C3 overexpression lines accumulated less. Our results suggest that MeSA glucosylation by UGT71C3 facilitates negative regulation of the SAR response by modulating homeostasis of MeSA and SA. This study unveils further SAR regulation mechanisms and highlights the role of glucosylation of MeSA and potentially other systemic signals in negatively modulating plant systemic defense.

Ectopic expression of glycosyltransferase UGT76E11 increases flavonoid accumulation and enhances abiotic stress tolerance in Arabidopsis.

Although plant glycosyltransferases are thought to play important roles in growth and interaction with the environment, little is known about their physiological roles for most members of the plant glycosyltransferase family. We cloned and characterised an Arabidopsis glycosyltransferase gene, UGT76E11. Its in vivo physiological effects on flavonoid accumulation and plant tolerance to abiotic stresses were investigated. The UGT76E11 gene was up-regulated in transcription expression under stress conditions of salinity, drought and H2 O2 treatment. Transgenic plants ectopically overexpressing UGT76E11 showed substantially enhanced tolerance to salinity and drought at germination and during post-germination growth. Enzyme activity of UGT76E11 to glucosylate quercetin and other flavonoids was confirmed. Ectopic expression of UGT76E11 resulted in significantly increased flavonoid content in transgenic plants compared to wild type, suggesting a contribution of UGT76E11 to modulation of flavonoid metabolism. Consistent with this result, several biosynthesis genes in the flavonoid pathway were clearly up-regulated in transgenic plants. Furthermore, overexpression of UGT76E11 also enhanced the scavenging capacity for ROS and increased expression levels of a number of stress-related genes. Based on these results, we suggest that the glycosyltransferase UGT76E11 plays an important role in modulating flavonoid metabolism and enhancing plant adaptation to environmental stresses. Our findings might allow use of glycosyltransferase UGT76E11 in crop improvement, towards both enhanced stress tolerance and increased flavonoid accumulation.

UDP-glycosyltransferase 72B1 catalyzes the glucose conjugation of monolignols and is essential for the normal cell wall lignification in Arabidopsis thaliana.

Glycosylation of monolignols has been found to be widespread in land plants since the 1970s. However, whether monolignol glycosylation is crucial for cell wall lignification and how it exerts effects are still unknown. Here, we report the identification of a mutant ugt72b1 showing aggravated and ectopic lignification in floral stems along with arrested growth and anthocyanin accumulation. Histochemical assays and thioacidolysis analysis confirmed the enhanced lignification and increased lignin biosynthesis in the ugt72b1 mutant. The loss of UDP-glycosyltransferase UGT72B1 function was responsible for the lignification phenotype, as demonstrated by complementation experiments. Enzyme activity analysis indicated that UGT72B1 could catalyze the glucose conjugation of monolignols, especially coniferyl alcohol and coniferyl aldehyde, which was confirmed by analyzing monolignol glucosides of UGT72B1 transgenic plants. Furthermore, the UGT72B1 gene was strongly expressed in young stem tissues, especially xylem tissues. However, UGT72B1 paralogs, such as UGT72B2 and UGT72B3, had weak enzyme activity toward monolignols and weak expression in stem tissues. Transcriptomic profiling showed that UGT72B1 knockout resulted in extensively increased transcript levels of genes involved in monolignol biosynthesis, lignin polymerization and cell wall-related transcription factors, which was confirmed by quantitative real-time PCR assays. These results provided evidence that monolignol glucosylation catalyzed by UGT72B1 was essential for normal cell wall lignification, thus offering insight into the molecular mechanism of cell wall development and cell wall lignification.