Heat shock protein 70 is required for tabtoxinine-β-lactam-induced cell death in Nicotiana benthamiana

Bibliographische Detailangaben
Veröffentlicht in:	Journal of plant physiology. - 1979. - 171(2014), 2 vom: 15. Jan., Seite 173-8
1. Verfasser:	Ito, Makoto (VerfasserIn)
Weitere Verfasser:	Yamamoto, Yu, Kim, Chul-Sa, Ohnishi, Kouhei, Hikichi, Yasufumi, Kiba, Akinori
Format:	Online-Aufsatz
Sprache:	English
Veröffentlicht:	2014
Zugriff auf das übergeordnete Werk:	Journal of plant physiology
Schlagworte:	Journal Article Research Support, Non-U.S. Gov't Cell death HR Heat shock protein 70 Hsp MSX Nicotiana benthamiana PCD PCR mehr... RT-PCR Tabtoxinine-β-lactam TβL VIGS Virus-induced gene silencing heat shock protein hypersensitive response l-methionine sulfoximine polymerase chain reaction programmed cell death qRT-PCR quantitative real time polymerase chain reaction reverse transcription-polymerase chain reaction tabtoxinine-β-lactam virus-induced gene silencing Azetidines Bacterial Toxins HSP70 Heat-Shock Proteins Methionine Sulfoximine 1982-67-8 tabtoxinine beta-lactam 65709-93-5 Glutamate-Ammonia Ligase EC 6.3.1.2

Beschreibung
Zusammenfassung:	Copyright © 2013 Elsevier GmbH. All rights reserved. Tabtoxinine-β-lactam (TβL), a non-specific bacterial toxin, is produced by Pseudomonas syringae pv. tabaci, the causal agent of tobacco wildfire disease. TβL causes death of plant cells through the inhibition of glutamine synthetase, which leads to an abnormal accumulation of ammonium ions and the characteristic necrotic wildfire lesions. To better understand the mechanisms involved in TβL-induced cell death, we studied its regulation in Nicotiana benthamiana. TβL-induced lesions, similar to those in controls, could be observed in SGT1-, RAR1- and Hsp90-silenced plants. In contrast, Hsp70-silenced plants showed suppression of lesion formation. Expression of hin1, a marker gene for the hypersensitive response (HR), which is a characteristic of programmed cell death in plants, was strongly induced in controls by TβL treatment but only slightly in Hsp70-silenced plants. However, in these TβL-treated Hsp70-silenced plants, the amount of ammonium ions was considerably increased. Furthermore, the silencing of Hsp70 also suppressed l-methionine sulfoximine-induced cell death and hin1 expression and caused the over-accumulation of ammonium ions. When inoculated directly with P. syringae pv. tabaci, Hsp70-silenced plants showed only reduced symptoms. Our results suggest that the TβL-induced pathway to cell death in N. benthamiana is at least partially similar to HR response, and that Hsp70 might play an essential role in these events
Beschreibung:	Date Completed 02.09.2014 Date Revised 13.12.2023 published: Print-Electronic Citation Status MEDLINE
ISSN:	1618-1328
DOI:	10.1016/j.jplph.2013.10.012