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Hindi Research Article
Chitin Elicitor-Responsive Photon Emission is potentiated by Plant Activators through Priming of Salicylic Acid Signaling via OsWRKY45 in Rice
Hiroyuki Iyozumi*, Hideki Nukui and Kimihiko Kato
Shizuoka Prefectural Research Institute of Agriculture and Forestry, Tomigaoka, Iwata, Shizuoka 438-0803, Japan
- *Corresponding Author:
- Hiroyuki Iyozumi
Shizuoka Prefectural Research Institute of Agriculture and Forestry
Tomigaoka, Iwata
Shizuoka 438-0803, Japan
Tel: +81 538 36 1556
Fax: +81 538 37 8466
E-mail: hiroyuki1_iyozumi@pref.shizuoka.lg.jp
Received date: July 15, 2016; Accepted date: September 09, 2016; Published date: September 16, 2016
Citation: Iyozumi H, Nukui H, Kato K (2016) Chitin Elicitor-Responsive Photon Emission is potentiated by Plant Activators through Priming of Salicylic Acid Signaling via OsWRKY45 in Rice. J Rice Res 4:175. doi:10.4172/2375-4338.1000175
Copyright: © 2016 Iyozumi H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Priming of plant cells for faster and enhanced defense responses against pathogen attacks is a common feature of chemically or biologically induced resistance. The authors previously developed a priming detection system that detects priming as potentiation of chitin elicitor-responsive photon emission (C-ERPE) in rice cells pretreated with various types of chemical inducers of disease resistance, called plant activators. To elucidate the mechanisms underlying C-ERPE potentiation, the authors performed gene knockdown of OsWRKY45, a major regulator of salicylic acid (SA)-dependent defense responses in rice, and estimated the effects of SA isomers on C-ERPE potentiation. Plant activators induced a 200-300% increase in C-ERPE in the wild type, whereas OsWRKY45 knockdown attenuated the increase in C-ERPE to less than 60%. Native SA induced more than a 150% increase in C-ERPE, but structural isomers of SA were less effective (10-24% increase). These SA signaling-disruption experiments indicate that the potentiation of C-ERPE requires intrinsic components of hormonal signaling for defense, at least for priming by inducers of systemic acquired resistance.
