Little is known about long‐distance mesophyll‐driven signals that regulate stomatal conductance. Soluble and/or vapor‐phase molecules have been proposed. In this study, the involvement of the gaseous signal ethylene in the modulation of stomatal conductance in We present a diffusion model which indicates that gaseous signaling molecule/s with a shorter/direct diffusion pathway to guard cells are more probable for rapid mesophyll‐dependent stomatal conductance changes. We, therefore, analyzed different Arabidopsis ethylene‐signaling and biosynthesis mutants for their ethylene production and kinetics of stomatal responses to ABA/[CO2]‐shifts. According to our research, higher [CO2] causes Arabidopsis rosettes to produce more ethylene. An ACC‐synthase octuple mutant with reduced ethylene biosynthesis exhibits dysfunctional CO2‐induced stomatal movements. Ethylene‐insensitive receptor (gain‐of‐function), These findings suggest essential functions of ethylene biosynthesis and signaling components in tuning/accelerating stomatal conductance responses to CO2and ABA.
Jasmonic acid (JA) and salicylic acid (SA) regulate stomatal closure, preventing pathogen invasion into plants. However, to what extent abscisic acid (ABA), SA and JA interact, and what the roles of SA and JA are in stomatal responses to environmental cues, remains unclear. Here, by using intact plant gas‐exchange measurements in JA and SA single and double mutants, we show that stomatal responsiveness to CO2, light intensity, ABA, high vapor pressure deficit and ozone either did not or, for some stimuli only, very slightly depended upon JA and SA biosynthesis and signaling mutants, including
- Award ID(s):
- 1900567
- NSF-PAR ID:
- 10449362
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- The Plant Journal
- Volume:
- 108
- Issue:
- 1
- ISSN:
- 0960-7412
- Page Range / eLocation ID:
- p. 134-150
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Summary Arabidopsis thaliana by CO2/abscisic acid (ABA) was examined.etr1‐1 andetr2‐1 , and signaling,ein2‐5 andein2‐1 , mutants showed intact stomatal responses to [CO2]‐shifts, whereas loss‐of‐function ethylene receptor mutants, includingetr2‐3;ein4‐4;ers2‐3 ,etr1‐6;etr2‐3 andetr1‐6 , showed markedly accelerated stomatal responses to [CO2]‐shifts. Further investigation revealed a significantly impaired stomatal closure to ABA in the ACC‐synthase octuple mutant and accelerated stomatal responses in theetr1‐6;etr2‐3 , andetr1‐6 , but not in theetr2‐3;ein4‐4;ers2‐3 mutants. -
Summary Respiration in leaves and the continued elevation in the atmospheric
CO 2concentration causeCO 2‐mediated reduction in stomatal pore apertures. Several mutants have been isolated for which stomatal responses to both abscisic acid (ABA ) andCO 2are simultaneously defective. However, there are only few mutations that impair the stomatal response to elevatedCO 2, but not toABA . Such mutants are invaluable in unraveling the molecular mechanisms of earlyCO 2signal transduction in guard cells. Recently, mutations in the mitogen‐activated protein (MAP ) kinase, , have been shown to partially impairMPK 12CO 2‐induced stomatal closure. Here, we show thatmpk12 plants, in which is stably silenced specifically in guard cells (MPK 4mpk12 mpk4 homozygous double‐mutants), completely lackGC CO 2‐induced stomatal responses and have impaired activation of guard cell S‐type anion channels in response to elevatedCO 2/bicarbonate. However,ABA ‐induced stomatal closure, S‐type anion channel activation andABA ‐induced marker gene expression remain intact in thempk12 mpk4 double‐mutants. These findings suggest thatGC MPK 12 andMPK 4 act very early inCO 2signaling, upstream of, or parallel to the convergence ofCO 2andABA signal transduction. The activities ofMPK 4 andMPK 12 protein kinases were not directly modulated byCO 2/bicarbonatein vitro , suggesting that they are not directCO 2/bicarbonate sensors. Further data indicate thatMPK 4 andMPK 12 have distinguishable roles in Arabidopsis and that the previously suggested role ofRHC 1 in stomatalCO 2signaling is minor, whereasMPK 4 andMPK 12 act as key components of early stomatalCO 2signal transduction. -
Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO2]. CO2elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO2/ABA interaction remain unclear. Two models have been considered: (
i ) CO2elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (ii ) CO2signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutantsnced3/nced5 andaba2-1 remain responsive to CO2elevation. Rapid CO2-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO2elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO2activates guard cell S-type anion channels innced3/nced5 and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO2does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO2signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO2. These findings provide insights into the interaction between CO2/ABA signal transduction in light of the continuing rise in atmospheric [CO2]. -
Summary Low concentrations of CO2cause stomatal opening, whereas [CO2] elevation leads to stomatal closure. Classical studies have suggested a role for Ca2+and protein phosphorylation in CO2‐induced stomatal closing. Calcium‐dependent protein kinases (CPKs) and calcineurin‐B‐like proteins (CBLs) can sense and translate cytosolic elevation of the second messenger Ca2+into specific phosphorylation events. However, Ca2+‐binding proteins that function in the stomatal CO2response remain unknown.
Time‐resolved stomatal conductance measurements using intact plants, and guard cell patch‐clamp experiments were performed.
We isolated
cpk quintuple mutants and analyzed stomatal movements in response to CO2, light and abscisic acid (ABA). Interestingly, we found thatcpk3/5/6/11/23 quintuple mutant plants, but not other analyzedcpk quadruple/quintuple mutants, were defective in high CO2‐induced stomatal closure and, unexpectedly, also in low CO2‐induced stomatal opening. Furthermore, K+‐uptake‐channel activities were reduced incpk3/5/6/11/23 quintuple mutants, in correlation with the stomatal opening phenotype. However, light‐mediated stomatal opening remained unaffected, and ABA responses showed slowing in some experiments. By contrast, CO2‐regulated stomatal movement kinetics were not clearly affected in plasma membrane‐targetedcbl1/4/5/8/9 quintuple mutant plants.Our findings describe combinatorial
cpk mutants that function in CO2control of stomatal movements and support the results of classical studies showing a role for Ca2+in this response. -
Summary Cytosolic calcium concentration ([Ca2+]cyt) and heterotrimeric G‐proteins are universal eukaryotic signaling elements. In plant guard cells, extracellular calcium (Cao) is as strong a stimulus for stomatal closure as the phytohormone abscisic acid (
ABA ), but underlying mechanisms remain elusive. Here, we report that the sole Arabidopsis heterotrimeric Gβ subunit,AGB 1, is required for four guard cell Caoresponses: induction of stomatal closure; inhibition of stomatal opening; [Ca2+]cytoscillation; and inositol 1,4,5‐trisphosphate (InsP3) production. Stomata in wild‐type Arabidopsis (Col) and in mutants of the canonical Gα subunit, , showed inhibition of stomatal opening and promotion of stomatal closure by Cao. By contrast, stomatal movements ofGPA 1agb1 mutants andagb1 /gpa1 double‐mutants, as well as those of theagg1agg2 Gγ double‐mutant, were insensitive to Cao. These behaviors contrast withABA ‐regulated stomatal movements, which involveGPA 1 andAGB 1/AGG 3 dimers, illustrating differential partitioning of G‐protein subunits among stimuli with similar ultimate impacts, which may facilitate stimulus‐specific encoding. knockouts retained reactive oxygen species andAGB 1NO production, but lostYC 3.6‐detected [Ca2+]cytoscillations in response to Cao, initiating only a single [Ca2+]cytspike. Experimentally imposed [Ca2+]cytoscillations restored stomatal closure inagb1 . Yeast two‐hybrid and bimolecular complementation fluorescence experiments revealed thatAGB 1 interacts with phospholipase Cs (PLCs), and Caoinduced InsP3 production in Col but not inagb1 . In sum, G‐protein signaling viaAGB 1/AGG 1/AGG 2 is essential for Cao‐regulation of stomatal apertures, and stomatal movements in response to Caoapparently require Ca2+‐induced Ca2+release that is likely dependent on Gβγ interaction withPLC s leading to InsP3 production.