TY - JOUR
T1 - Association between Ion Fluxes and Defense Responses in Pea and Cowpea Tissues
AU - Amano, Masashi
AU - Toyoda, Kazuhiro
AU - Ichinose, Yuki
AU - Yamada, Tetsuji
AU - Shiraishi, Tomonori
N1 - Funding Information:
The authors are grateful to Prof. T. Shimmen of the Himeji Institute for Technology, for his valuable suggestions during the preparation of the manuscript. They are also indebted to Ms. Y. Yamaguchi and Mr. Y. Todo for their skilled technical assistance. This research was supported in part by the Grant from the Japan Society for the Promotion of Science Research for the Future Program (JSPS-RFTF96L00603) and the Grants-in-Aid from the Ministry of Education, Science and Culture of Japan. Financial support from Sankyo Co. Ltd. Tokyo, Japan, and the Institute for Life Science Research and Development, Okayama, Japan, is also acknowledged.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1997/6
Y1 - 1997/6
N2 - The glycopeptide elicitor from a pea pathogen, Mycosphaerella pinodes, induced rapid alkalinization and increases in levels of Na+ and K+ ions in the extracellular solution upon contact with pea and cowpea tissues. The presence of monensin, nigericin, lidocaine, quinidine or phenytoin together with the elicitor markedly inhibited these changes, whereas the presence of valinomycin, gramicidin D, tetraethylammonium, CsCl and aminopyridine did not. The production of phytoalexins in pea and cowpea tissues was also strongly inhibited by the simultaneous presence of the former reagents but not of the latter reagents. Inhibitory effects on the production of phytoalexins were diminished when monensin, nigericin or a Na+-channel blocker was applied 3 h after the start of treatment with elicitor. Furthermore, orthovanadate and neomycin, which suppress defense responses in both tissues, also inhibited the above mentioned changes. By contrast, the species-specific suppressor from M. pinodes inhibited the elicitor-induced release of Na+ and K+ ions from pea tissues, but, conversely, by itself it elicited either the defense response or the release of Na+ and K+ ions from cowpea tissues. The results indicate that these ion-related changes, in particular the efflux of Na+ and K+ ions, might be closely associated with the signal transduction system for defense responses at the tissue level.
AB - The glycopeptide elicitor from a pea pathogen, Mycosphaerella pinodes, induced rapid alkalinization and increases in levels of Na+ and K+ ions in the extracellular solution upon contact with pea and cowpea tissues. The presence of monensin, nigericin, lidocaine, quinidine or phenytoin together with the elicitor markedly inhibited these changes, whereas the presence of valinomycin, gramicidin D, tetraethylammonium, CsCl and aminopyridine did not. The production of phytoalexins in pea and cowpea tissues was also strongly inhibited by the simultaneous presence of the former reagents but not of the latter reagents. Inhibitory effects on the production of phytoalexins were diminished when monensin, nigericin or a Na+-channel blocker was applied 3 h after the start of treatment with elicitor. Furthermore, orthovanadate and neomycin, which suppress defense responses in both tissues, also inhibited the above mentioned changes. By contrast, the species-specific suppressor from M. pinodes inhibited the elicitor-induced release of Na+ and K+ ions from pea tissues, but, conversely, by itself it elicited either the defense response or the release of Na+ and K+ ions from cowpea tissues. The results indicate that these ion-related changes, in particular the efflux of Na+ and K+ ions, might be closely associated with the signal transduction system for defense responses at the tissue level.
KW - Defense response
KW - Elicitor
KW - Ion flux
KW - Pisum sativum L.
KW - Suppressor
KW - Vigna sinensis endl
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U2 - 10.1093/oxfordjournals.pcp.a029223
DO - 10.1093/oxfordjournals.pcp.a029223
M3 - Article
C2 - 9249987
AN - SCOPUS:0031154190
SN - 0032-0781
VL - 38
SP - 698
EP - 706
JO - Plant and Cell Physiology
JF - Plant and Cell Physiology
IS - 6
ER -