Chitosan signaling in guard cells requires endogenous salicylic acid

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

An elicitor chitosan (CHT) induces stomatal closure but the mechanism remains to be clarified. A phytohormone salicylic acid (SA) is crucial for elicitor-induced defense signaling in plants. Here we investigated whether endogenous SA is required for CHT signaling in guard cells. In the SA-deficient nahG mutant, treatment of CHT did not induce either apoplastic reactive oxygen species (ROS) production or stomatal closure but co-treatment of CHT and SA induced both apoplastic ROS production and stomatal closure, indicating the involvement of endogenous SA in CHT-induced apoplastic ROS production and CHT-induced stomatal closure. Furthermore, CHT induced transient cytosolic free calcium concentration increments in the nahG mutant in the presence of exogenous SA but not in the absence of exogenous SA. These results provide evidence that endogenous SA is a crucial element in CHT-induced stomatal closure.

Original languageEnglish
Pages (from-to)1536-1541
Number of pages6
JournalBioscience, Biotechnology and Biochemistry
Volume81
Issue number8
DOIs
Publication statusPublished - 2017

Fingerprint

Salicylic Acid
Chitosan
Reactive Oxygen Species
Plant Growth Regulators
Calcium

Keywords

  • Chitosan
  • Cytosolic Ca oscillations
  • Reactive oxygen species
  • Salicylic acid
  • Stomatal closure

ASJC Scopus subject areas

  • Analytical Chemistry
  • Biotechnology
  • Biochemistry
  • Applied Microbiology and Biotechnology
  • Molecular Biology
  • Organic Chemistry

Cite this

Chitosan signaling in guard cells requires endogenous salicylic acid. / Prodhan, Md Yeasin; Issak, Mohammad; Nakamura, Toshiyuki; Munemasa, Shintaro; Nakamura, Yoshimasa; Murata, Yoshiyuki.

In: Bioscience, Biotechnology and Biochemistry, Vol. 81, No. 8, 2017, p. 1536-1541.

Research output: Contribution to journalArticle

@article{b265258aa91b44219a1dbb18db25a910,
title = "Chitosan signaling in guard cells requires endogenous salicylic acid",
abstract = "An elicitor chitosan (CHT) induces stomatal closure but the mechanism remains to be clarified. A phytohormone salicylic acid (SA) is crucial for elicitor-induced defense signaling in plants. Here we investigated whether endogenous SA is required for CHT signaling in guard cells. In the SA-deficient nahG mutant, treatment of CHT did not induce either apoplastic reactive oxygen species (ROS) production or stomatal closure but co-treatment of CHT and SA induced both apoplastic ROS production and stomatal closure, indicating the involvement of endogenous SA in CHT-induced apoplastic ROS production and CHT-induced stomatal closure. Furthermore, CHT induced transient cytosolic free calcium concentration increments in the nahG mutant in the presence of exogenous SA but not in the absence of exogenous SA. These results provide evidence that endogenous SA is a crucial element in CHT-induced stomatal closure.",
keywords = "Chitosan, Cytosolic Ca oscillations, Reactive oxygen species, Salicylic acid, Stomatal closure",
author = "Prodhan, {Md Yeasin} and Mohammad Issak and Toshiyuki Nakamura and Shintaro Munemasa and Yoshimasa Nakamura and Yoshiyuki Murata",
year = "2017",
doi = "10.1080/09168451.2017.1332979",
language = "English",
volume = "81",
pages = "1536--1541",
journal = "Bioscience, Biotechnology and Biochemistry",
issn = "0916-8451",
publisher = "Japan Society for Bioscience Biotechnology and Agrochemistry",
number = "8",

}

TY - JOUR

T1 - Chitosan signaling in guard cells requires endogenous salicylic acid

AU - Prodhan, Md Yeasin

AU - Issak, Mohammad

AU - Nakamura, Toshiyuki

AU - Munemasa, Shintaro

AU - Nakamura, Yoshimasa

AU - Murata, Yoshiyuki

PY - 2017

Y1 - 2017

N2 - An elicitor chitosan (CHT) induces stomatal closure but the mechanism remains to be clarified. A phytohormone salicylic acid (SA) is crucial for elicitor-induced defense signaling in plants. Here we investigated whether endogenous SA is required for CHT signaling in guard cells. In the SA-deficient nahG mutant, treatment of CHT did not induce either apoplastic reactive oxygen species (ROS) production or stomatal closure but co-treatment of CHT and SA induced both apoplastic ROS production and stomatal closure, indicating the involvement of endogenous SA in CHT-induced apoplastic ROS production and CHT-induced stomatal closure. Furthermore, CHT induced transient cytosolic free calcium concentration increments in the nahG mutant in the presence of exogenous SA but not in the absence of exogenous SA. These results provide evidence that endogenous SA is a crucial element in CHT-induced stomatal closure.

AB - An elicitor chitosan (CHT) induces stomatal closure but the mechanism remains to be clarified. A phytohormone salicylic acid (SA) is crucial for elicitor-induced defense signaling in plants. Here we investigated whether endogenous SA is required for CHT signaling in guard cells. In the SA-deficient nahG mutant, treatment of CHT did not induce either apoplastic reactive oxygen species (ROS) production or stomatal closure but co-treatment of CHT and SA induced both apoplastic ROS production and stomatal closure, indicating the involvement of endogenous SA in CHT-induced apoplastic ROS production and CHT-induced stomatal closure. Furthermore, CHT induced transient cytosolic free calcium concentration increments in the nahG mutant in the presence of exogenous SA but not in the absence of exogenous SA. These results provide evidence that endogenous SA is a crucial element in CHT-induced stomatal closure.

KW - Chitosan

KW - Cytosolic Ca oscillations

KW - Reactive oxygen species

KW - Salicylic acid

KW - Stomatal closure

UR - http://www.scopus.com/inward/record.url?scp=85024494269&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85024494269&partnerID=8YFLogxK

U2 - 10.1080/09168451.2017.1332979

DO - 10.1080/09168451.2017.1332979

M3 - Article

C2 - 28585465

AN - SCOPUS:85024494269

VL - 81

SP - 1536

EP - 1541

JO - Bioscience, Biotechnology and Biochemistry

JF - Bioscience, Biotechnology and Biochemistry

SN - 0916-8451

IS - 8

ER -