Premium
Strigolactone‐triggered stomatal closure requires hydrogen peroxide synthesis and nitric oxide production in an abscisic acid‐independent manner
Author(s) -
Lv Shuo,
Zhang Yonghong,
Li Chen,
Liu Zhijun,
Yang Nan,
Pan Lixia,
Wu Jinbin,
Wang Jiajing,
Yang Jingwei,
Lv Yanting,
Zhang Yutao,
Jiang Wenqian,
She Xiaoping,
Wang Guodong
Publication year - 2018
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14813
Subject(s) - guard cell , abscisic acid , strigolactone , mutant , nitric oxide , hydrogen peroxide , arabidopsis , abiotic stress , salicylic acid , acclimatization , microbiology and biotechnology , chemistry , botany , biology , biochemistry , gene , organic chemistry
Summary Accumulating data indicate that strigolactones ( SL s) are implicated in the response to environmental stress, implying a potential effect of SL s on stomatal response and thus stress acclimatization. In this study, we investigated the molecular mechanism underlying the effect of SLs on stomatal response and their interrelation with abscisic acid ( ABA ) signaling. The impact of SL s on the stomatal response was investigated by conducting SL ‐feeding experiments and by analyzing SL ‐related mutants. The involvement of endogenous ABA and ABA ‐signaling components in SL ‐mediated stomatal closure was physiologically evaluated using genetic mutants. Pharmacological and genetic approaches were employed to examine hydrogen peroxide (H 2 O 2 ) and nitric oxide ( NO ) production. SL ‐related mutants exhibited larger stomatal apertures, while exogenous SL s were able to induce stomatal closure and rescue the more widely opening stomata of SL ‐deficient mutants. The SL ‐biosynthetic genes were induced by abiotic stress in shoot tissues. Disruption of ABA ‐biosynthetic genes, as well as genes that function in guard cell ABA signaling, resulted in no impairment in SL ‐mediated stomatal response. However, disruption of MORE AXILLARY GROWTH2 ( MAX 2 ), DWARF14 ( D14 ), and the anion channel gene SLOW ANION CHANNEL‐ASSOCIATED 1 (SLAC1) impaired SL ‐triggered stomatal closure. SL s stimulated a marked increase in H 2 O 2 and NO contents, which is required for stomatal closure. Our results suggest that SL s play a prominent role, together with H 2 O 2 / NO production and SLAC 1 activation, in inducing stomatal closure in an ABA ‐independent mechanism.