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 language | English |
|---|---|
| Pages (from-to) | 167-170 |
| Number of pages | 4 |
| Journal | Journal of Plant Physiology |
| Volume | 218 |
| DOIs | |
| Publication status | Published - Nov 1 2017 |
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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 journal › Article
}
TY - JOUR
T1 - Phosphoinositide 3-kinase participates in L-methionine sulfoximine-induced cell death via salicylic acid mediated signaling in Nicotiana benthamiana
AU - Sumida, Sayuri
AU - Ito, Makoto
AU - Galis, Ivan
AU - Nakatani, Hiroko
AU - Shinya, Tomonori
AU - Ohnishi, Kouhei
AU - Hikichi, Yasufumi
AU - Kiba, Akinori
PY - 2017/11/1
Y1 - 2017/11/1
N2 - 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.
AB - 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.
KW - L-Methionine sulfoximine
KW - Nicotiana benthamiana
KW - Phosphoinositide 3-kinase
KW - Programmed cell death
KW - Salicylic acid
KW - Wildfire disease
UR - http://www.scopus.com/inward/record.url?scp=85028574213&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85028574213&partnerID=8YFLogxK
U2 - 10.1016/j.jplph.2017.07.016
DO - 10.1016/j.jplph.2017.07.016
M3 - Article
C2 - 28866325
AN - SCOPUS:85028574213
VL - 218
SP - 167
EP - 170
JO - Journal of Plant Physiology
JF - Journal of Plant Physiology
SN - 0176-1617
ER -