Phosphoinositide 3-kinase participates in L-methionine sulfoximine-induced cell death via salicylic acid mediated signaling in Nicotiana benthamiana

Sayuri Sumida, Makoto Ito, Ivan Galis, Hiroko Nakatani, Tomonori Shinya, Kouhei Ohnishi, Yasufumi Hikichi, Akinori Kiba

Research output: Contribution to journalArticle

Abstract

Pseudomonas syringae pv. tabaci causes wildfire disease by the action of tabtoxinine-β-lactam (TβL), 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 TβL 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 TβL-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 TβL action in N. benthamiana.

Original languageEnglish
Pages (from-to)167-170
Number of pages4
JournalJournal of Plant Physiology
Volume218
DOIs
Publication statusPublished - Nov 1 2017

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Methionine Sulfoximine
lactams
Lactams
1-Phosphatidylinositol 4-Kinase
Salicylic Acid
Nicotiana benthamiana
phosphatidylinositol 3-kinase
salicylic acid
Methionine
lesions (plant)
Tobacco
methionine
cell death
Cell Death
Pseudomonas syringae pv. tabaci
Pseudomonas syringae
bacterial toxins
Bacterial Toxins
ammonium compounds
genetic markers

Keywords

  • L-Methionine sulfoximine
  • Nicotiana benthamiana
  • Phosphoinositide 3-kinase
  • Programmed cell death
  • Salicylic acid
  • Wildfire disease

ASJC Scopus subject areas

  • Physiology
  • Agronomy and Crop Science
  • Plant Science

Cite this

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.

In: Journal of Plant Physiology, Vol. 218, 01.11.2017, p. 167-170.

Research output: Contribution to journalArticle

Sumida, Sayuri ; Ito, Makoto ; Galis, Ivan ; Nakatani, Hiroko ; Shinya, Tomonori ; Ohnishi, Kouhei ; Hikichi, Yasufumi ; Kiba, Akinori. / Phosphoinositide 3-kinase participates in L-methionine sulfoximine-induced cell death via salicylic acid mediated signaling in Nicotiana benthamiana. In: Journal of Plant Physiology. 2017 ; Vol. 218. pp. 167-170.
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abstract = "Pseudomonas syringae pv. tabaci causes wildfire disease by the action of tabtoxinine-β-lactam (TβL), 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 TβL 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 TβL-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 TβL action in N. benthamiana.",
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AU - Ito, Makoto

AU - Galis, Ivan

AU - Nakatani, Hiroko

AU - Shinya, Tomonori

AU - Ohnishi, Kouhei

AU - Hikichi, Yasufumi

AU - Kiba, Akinori

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