| 研究実績の概要 |
Plants protect themselves from harmful gases through closing stomata and/or detoxification. Sulfur dioxide (SO2) is a harmful gas known to induce stomatal closure. However, the cellular mechanism mediating SO2-induced stomatal closure remains obscure.
To shed lights on the roles of phytohormones in SO2-induced closure, we examined the temporal patterns of nine phytohormones, gibberellin A1, A4, abscisic acid, salicylic acid, jasmonic acid (JA), jasmonoylisoleucine (JA-Ile), indoleacetic acid, zeatin and isopentenyladenine in SO2-treated plants. The contents of JA and JA-Ile continuously increased.
Through comparison of estimated atmospheric concentrations of these gases along the evolution of plants, we propose that this difference is attributed to historical difference in the gas compositions in the atmosphere. Sulfite oxidase (SO) is the key enzyme in SO2 detoxification. Phylogenetic analysis revealed that SO has evolutionally developed dating back at least to green algae. We understand that the detoxification mechanism against SO2 evolved earlier than stomatal defense.
We hypothesized that the action of SO2 inducing stomata is through acidosis. AtClCa is a nitrate/proton antiporter mediating pH stabilization of guard cells. We found that clca mutant guard cells demonstrated stronger resistance to SO2 than guard cells of wild-type plants.
|
| 現在までの達成度 (区分) |
現在までの達成度 (区分)
2: おおむね順調に進展している
理由
Our quantitative analysis of nine phytohormones revealed that JA, JA-Ile and IAA contents were changed by SO2 exposure. We scrutinized the involvement of JA and JA-Ile using a JA insensitive mutant, coi1. This work suggested no involvement of JA in SO2-induced stomatal closure. On the other hand, the observation of a transient increment in IAA level where SO2-induced stomatal closure occurred suggests its novel role in inducing stomatal closure.
Hydrogen sulfide (H2S) and nitric oxide (NO) have been suggested to participate in SO2-induced stomatal closure in sweet potato in a past study. We investigated the involvement of H2S and NO in Arabidopsis and found that neither H2S or NO were involved in this process. Our pharmacological study also denied the involvement of reactive oxygen species on SO2-induced stomatal closure, which have been anticipated in a past study.
We also conducted bioinformatics research on the relationship of atmospheric concentration of air pollutants and development of plant defense mechanisms. Our results suggested that guard cell signaling mechanism to ozone and carbon dioxide may be co-established with the acquirement of stomatal apparatus, but SO2 may be far recent. However, SO2 detoxification mechanism of plants had already been developed in algae.
Our hypothesis that SO2 toxicity to guard cells is mediated by acidosis is currently tested by a pH homeostasis mutant, clca. The preliminary study shows a promising result. This will be confirmed in the next 6 months.
Above progresses reasonably fit to the research plan.
|
