Exogenous application of L‐histidine suppresses bacterial diseases and enhances ethylene production in rice seedlings
Exogenous application of L‐histidine suppresses bacterial diseases and enhances ethylene production in rice seedlings
复制标题
外源施用L-组氨酸抑制细菌性病害并提高水稻幼苗乙烯产量
DOI:
10.1111/ppa.13037
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发表时间:
2019
期刊:
影响因子:
2.7
通讯作者:
Takahashi H.
中科院分区:
文献类型:
--
作者:
Yariyama S.;Ando S.;Seo S.;Nakaho K.;Miyashita S.;Kanayama Y.;Takahashi H.
Exogenous application ofl‐histidine enhances resistance to pathogens in tomato (Solanum lycopersicum) andArabidopsis thalianavia activation of the ethylene (ET)‐dependent signalling pathway. In this study, the efficacy ofl‐histidine for suppression of bacterial diseases in rice seedlings was investigated. Rice seeds were soaked in 10 mm l‐histidine, 10 mm l‐lysine, or distilled water (DW) as a control for 48 h at 28 °C to stimulate germination. Treated seeds were then vacuum‐inoculated withBurkholderia glumaeorB. plantarii. Seedling diseases caused by both of these bacterial pathogens were suppressed by treatment withl‐histidine but not by treatment withl‐lysine or DW. Expression of an ET‐responsive defence‐related gene,OsGLP8‐12, was induced by treatment of seeds withl‐histidine. As diseases were not suppressed in rice seedlings treated withl‐histidine after vacuum‐inoculation, pretreatment of rice seedlings withl‐histidine before inoculation might activate the plant immune system. Indeed, ethylene production and the abundance of 1‐aminocyclopropane‐1‐carboxylic acid (ACC) synthase 2 (OsACS2) transcript increased in healthy seedlings grown from rice seeds treated withl‐histidine but not in those treated with DW. Furthermore, treatment of rice seeds with ACC, an ethylene precursor, suppressed bacterial rice seedling rot caused byB. glumaeas effectively as did treatment withl‐histidine, whereas treatment of rice seeds with aminooxyacetic acid, an inhibitor of ACC synthase, partially compromised disease suppression. Taken together,l‐histidine seems to suppress bacterial rice seedling diseases via an ethylene‐dependent resistance pathway.