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Phosphoinositide 3-kinase participates in l-methionine sulfoximine-induced cell death via salicylic acid mediated signaling in Nicotiana benthamiana.
Sumida, Sayuri; Ito, Makoto; Galis, Ivan; Nakatani, Hiroko; Shinya, Tomonori; Ohnishi, Kouhei; Hikichi, Yasufumi; Kiba, Akinori.
Afiliação
  • Sumida S; Laboratory of Plant Pathology and Biotechnology, Faculty of Agriculture, Kochi University, Nankoku 783-8502, Japan.
  • Ito M; Laboratory of Plant Pathology and Biotechnology, Faculty of Agriculture, Kochi University, Nankoku 783-8502, Japan.
  • Galis I; Institute of Plant Science and Resources, Okayama University, Okayama 710-0046, Japan.
  • Nakatani H; Institute of Plant Science and Resources, Okayama University, Okayama 710-0046, Japan.
  • Shinya T; Institute of Plant Science and Resources, Okayama University, Okayama 710-0046, Japan.
  • Ohnishi K; Research Institute of Molecular Genetics, Kochi University, Nankoku, Kochi 783-8502, Japan.
  • Hikichi Y; Laboratory of Plant Pathology and Biotechnology, Faculty of Agriculture, Kochi University, Nankoku 783-8502, Japan.
  • Kiba A; Laboratory of Plant Pathology and Biotechnology, Faculty of Agriculture, Kochi University, Nankoku 783-8502, Japan. Electronic address: akiba@kochi-u.ac.jp.
J Plant Physiol ; 218: 167-170, 2017 Nov.
Article em En | MEDLINE | ID: mdl-28866325
ABSTRACT
Pseudomonas syringae pv. tabaci causes wildfire disease by the action of tabtoxinine-ß-lactam (TßL), a non-specific bacterial toxin. To better understand the molecular mechanisms of wildfire disease and its development, we focused on the phosphoinositide 3-kinase in Nicotiana benthamiana (NbPI3K) and its potential role in the disease outbreak, using l-methionine sulfoximine (MSX) as an easily accessible mimic of the TßL action. The NbPI3K-silenced plants showed accelerated induction of cell death and necrotic lesion formation by MSX, and the expression of hin1, marker gene for the programmed cell death, was strongly induced in the plants. However, the accumulation of ammonium ions, caused by MSX inhibition of glutamine sythetase activity, was not affected by the NbPI3K-silencing. Interestingly, the expression of PR-1a, a marker gene for salicylic acid (SA) innate immunity signaling, and accumulation of SA were both enhanced in the NbPI3K-silenced plants. Accordingly, the acceleration of MSX-induced cell death by NbPI3K-silencing was reduced in NahG plants, and by double silencing of NbPI3K together with the NbICS1 encoding a SA-biosynthetic enzyme. As silencing of NbPI3K accelerated the TßL-induced necrotic lesions, and lesions of wildfire disease caused by P. syringae pv. tabaci, these results suggest that the NbPI3K-related pathway might act as a negative regulator of cell death during development of wildfire disease that involves SA-dependent signaling pathway downstream of TßL action in N. benthamiana.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas de Plantas / Nicotiana / Transdução de Sinais / Morte Celular / Ácido Salicílico / Fosfatidilinositol 3-Quinase / Metionina Sulfoximina Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas de Plantas / Nicotiana / Transdução de Sinais / Morte Celular / Ácido Salicílico / Fosfatidilinositol 3-Quinase / Metionina Sulfoximina Idioma: En Ano de publicação: 2017 Tipo de documento: Article