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Contribution of salicylic acid glucosyltransferase, OsSGT1, to chemically induced disease resistance in rice plants
Author(s) -
Umemura Kenji,
Satou Junji,
Iwata Michiaki,
Uozumi Nobuyuki,
Koga Jinichiro,
Kawano Tomonori,
Koshiba Tomokazu,
Anzai Hiroyuki,
Mitomi Masaaki
Publication year - 2009
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2008.03697.x
Subject(s) - salicylic acid , biology , glucosyltransferase , gene , gene silencing , plant disease resistance , gene expression , mediator , oryza sativa , biochemistry , microbiology and biotechnology
Summary Systemic acquired resistance (SAR), a natural disease response in plants, can be induced chemically. Salicylic acid (SA) acts as a key endogenous signaling molecule that mediates SAR in dicotyledonous plants. However, the role of SA in monocotyledonous plants has yet to be elucidated. In this study, the mode of action of the agrochemical protectant chemical probenazole was assessed by microarray‐based determination of gene expression. Cloning and characterization of the most highly activated probenazole‐responsive gene revealed that it encodes UDP‐glucose:SA glucosyltransferase (OsSGT1) , which catalyzes the conversion of free SA into SA O‐ β‐glucoside (SAG). We found that SAG accumulated in rice leaf tissue following treatment with probenazole or 2,6‐dichloroisonicotinic acid. A putative OsSGT1 gene from the rice cultivar Akitakomachi was cloned and the gene product expressed in Escherichia coli was characterized, and the results suggested that probenazole‐responsive OsSGT1 is involved in the production of SAG. Furthermore, RNAi‐mediated silencing of the OsSGT1 gene significantly reduced the probenazole‐dependent development of resistance against blast disease, further supporting the suggestion that OsSGT1 is a key mediator of development of chemically induced disease resistance. The OsSGT1 gene may contribute to the SA signaling mechanism by inducing up‐regulation of SAG in rice plants.