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Ye Yin Yuji Adachi Wenxiu Ye Maki Hayashi Yoshimasa Nakamura Toshinori Kinoshita Izumi C. Mori Yoshiyuki Murata 《Plant physiology》2013,161(2):600-616
Abscisic acid (ABA) induces stomatal closure and inhibits light-induced stomatal opening. The mechanisms in these two processes are not necessarily the same. It has been postulated that the ABA receptors involved in opening inhibition are different from those involved in closure induction. Here, we provide evidence that four recently identified ABA receptors (PYRABACTIN RESISTANCE1 [PYR1], PYRABACTIN RESISTANCE-LIKE1 [PYL1], PYL2, and PYL4) are not sufficient for opening inhibition in Arabidopsis (Arabidopsis thaliana). ABA-induced stomatal closure was impaired in the pyr1/pyl1/pyl2/pyl4 quadruple ABA receptor mutant. ABA inhibition of the opening of the mutant’s stomata remained intact. ABA did not induce either the production of reactive oxygen species and nitric oxide or the alkalization of the cytosol in the quadruple mutant, in accordance with the closure phenotype. Whole cell patch-clamp analysis of inward-rectifying K+ current in guard cells showed a partial inhibition by ABA, indicating that the ABA sensitivity of the mutant was not fully impaired. ABA substantially inhibited blue light-induced phosphorylation of H+-ATPase in guard cells in both the mutant and the wild type. On the other hand, in a knockout mutant of the SNF1-related protein kinase, srk2e, stomatal opening and closure, reactive oxygen species and nitric oxide production, cytosolic alkalization, inward-rectifying K+ current inactivation, and H+-ATPase phosphorylation were not sensitive to ABA.The phytohormone abscisic acid (ABA), which is synthesized in response to abiotic stresses, plays a key role in the drought hardiness of plants. Reducing transpirational water loss through stomatal pores is a major ABA response (Schroeder et al., 2001). ABA promotes the closure of open stomata and inhibits the opening of closed stomata. These effects are not simply the reverse of one another (Allen et al., 1999; Wang et al., 2001; Mishra et al., 2006).A class of receptors of ABA was identified (Ma et al., 2009; Park et al., 2009; Santiago et al., 2009; Nishimura et al., 2010). The sensitivity of stomata to ABA was strongly decreased in quadruple and sextuple mutants of the ABA receptor genes PYRABACTIN RESISTANCE/PYRABACTIN RESISTANCE-LIKE/REGULATORY COMPONENT OF ABSCISIC ACID RECEPTOR (PYR/PYL/RCAR; Nishimura et al., 2010; Gonzalez-Guzman et al., 2012). The PYR/PYL/RCAR receptors are involved in the early ABA signaling events, in which a sequence of interactions of the receptors with PROTEIN PHOSPHATASE 2Cs (PP2Cs) and subfamily 2 SNF1-RELATED PROTEIN KINASES (SnRK2s) leads to the activation of downstream ABA signaling targets in guard cells (Cutler et al., 2010; Kim et al., 2010; Weiner et al., 2010). Studies of Commelina communis and Vicia faba suggested that the ABA receptors involved in stomatal opening are not the same as the ABA receptors involved in stomatal closure (Allan et al., 1994; Anderson et al., 1994; Assmann, 1994; Schwartz et al., 1994). The roles of PYR/PYL/RCAR in either stomatal opening or closure remained to be elucidated.Blue light induces stomatal opening through the activation of plasma membrane H+-ATPase in guard cells that generates an inside-negative electrochemical gradient across the plasma membrane and drives K+ uptake through voltage-dependent inward-rectifying K+ channels (Assmann et al., 1985; Shimazaki et al., 1986; Blatt, 1987; Schroeder et al., 1987; Thiel et al., 1992). Phosphorylation of the penultimate Thr of the plasma membrane H+-ATPase is a prerequisite for blue light-induced activation of the H+-ATPase (Kinoshita and Shimazaki, 1999, 2002). ABA inhibits H+-ATPase activity through dephosphorylation of the penultimate Thr in the C terminus of the H+-ATPase in guard cells, resulting in prevention of the opening (Goh et al., 1996; Zhang et al., 2004; Hayashi et al., 2011). Inward-rectifying K+ currents (IKin) of guard cells are negatively regulated by ABA in addition to through the decline of the H+ pump-driven membrane potential difference (Schroeder and Hagiwara, 1989; Blatt, 1990; McAinsh et al., 1990; Schwartz et al., 1994; Grabov and Blatt, 1999; Saito et al., 2008). This down-regulation of ion transporters by ABA is essential for the inhibition of stomatal opening.A series of second messengers has been shown to mediate ABA-induced stomatal closure. Reactive oxygen species (ROS) produced by NADPH oxidases play a crucial role in ABA signaling in guard cells (Pei et al., 2000; Zhang et al., 2001; Kwak et al., 2003; Sirichandra et al., 2009; Jannat et al., 2011). Nitric oxide (NO) is an essential signaling component in ABA-induced stomatal closure (Desikan et al., 2002; Guo et al., 2003; Garcia-Mata and Lamattina, 2007; Neill et al., 2008). Alkalization of cytosolic pH in guard cells is postulated to mediate ABA-induced stomatal closure in Arabidopsis (Arabidopsis thaliana) and Pisum sativum and Paphiopedilum species (Irving et al., 1992; Gehring et al., 1997; Grabov and Blatt, 1997; Suhita et al., 2004; Gonugunta et al., 2008). These second messengers transduce environmental signals to ion channels and ion transporters that create the driving force for stomatal movements (Ward et al., 1995; MacRobbie, 1998; Garcia-Mata et al., 2003).In this study, we examined the mobilization of second messengers, the inactivation of IKin, and the suppression of H+-ATPase phosphorylation evoked by ABA in Arabidopsis mutants to clarify the downstream signaling events of ABA signaling in guard cells. The mutants included a quadruple mutant of PYR/PYL/RCARs, pyr1/pyl1/pyl2/pyl4, and a mutant of a SnRK2 kinase, srk2e. 相似文献
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Stomatal responses to vapor pressure deficit (VPD) are a principal means by which vascular land plants regulate daytime transpiration. While much work has focused on characterizing and modeling this response, there remains no consensus as to the mechanism that drives it. Explanations range from passive regulation by leaf hydration to biochemical regulation by the phytohormone abscisic acid (ABA). We monitored ABA levels, leaf gas exchange, and water status in a diversity of vascular land plants exposed to a symmetrical, mild transition in VPD. The stomata in basal lineages of vascular plants, including gymnosperms, appeared to respond passively to changes in leaf water status induced by VPD perturbation, with minimal changes in foliar ABA levels and no hysteresis in stomatal action. In contrast, foliar ABA appeared to drive the stomatal response to VPD in our angiosperm samples. Increased foliar ABA level at high VPD in angiosperm species resulted in hysteresis in the recovery of stomatal conductance; this was most pronounced in herbaceous species. Increased levels of ABA in the leaf epidermis were found to originate from sites of synthesis in other parts of the leaf rather than from the guard cells themselves. The transition from a passive regulation to ABA regulation of the stomatal response to VPD in the earliest angiosperms is likely to have had critical implications for the ecological success of this lineage.Plants continuously regulate transpiration by controlling the aperture of the stomatal pores on the surface of the leaf. The principal atmospheric determinant of stomatal aperture is the humidity of the air, which can be expressed as the vapor pressure difference between the leaf and the atmosphere. Stomatal responses to atmospheric vapor pressure deficit (VPD) have been well characterized across the diversity of vascular plant species (Darwin, 1898; Lange et al., 1971; Turner et al., 1984; Franks and Farquhar, 1999; Oren et al., 1999; Brodribb and McAdam, 2011; Mott and Peak, 2013), with stomata typically closing at high VPD and opening at low VPD. This comprehensive characterization has allowed for the development of highly effective empirical and mechanistic models of leaf gas exchange that provide robust predictions of the responses of transpiration to changes in VPD (Buckley et al., 2003; Katul et al., 2009; Damour et al., 2010; Medlyn et al., 2011). Despite the success of this modeling, the mechanism for the stomatal response to VPD remains poorly understood (Damour et al., 2010). Different hypotheses range from one extreme, whereby stomata respond passively through changes in leaf water content induced by the VPD or humidity perturbation (Lange et al., 1971; Mott and Peak, 2013), to the other extreme, whereby stomata close uniquely in response to the phytohormone abscisic acid (ABA; Xie et al., 2006; Bauer et al., 2013).From the earliest recognition that stomata open and close by changes in guard cell turgor (Heath, 1938), there have been many attempts to link the passive changes in water status that occur during VPD or humidity transitions with stomatal responses to VPD or humidity (Lange et al., 1971; Mott and Peak, 2013). Studies have suggested that changes in atmospheric water content passively drive stomatal responses by changing bulk leaf water status, which in turn changes guard cell turgor (Oren et al., 1999), or alternatively by changing guard cell turgor directly (Mott and Peak, 2013). Models based on these entirely passive processes are highly effective in predicting steady-state stomatal conductance (gs) in response to changes in VPD or humidity in angiosperms (Mott and Peak, 2013).While hydraulic models provide robust predictions of steady-state gs, they are less effective at predicting the dynamic responses of stomata to short-term perturbations, particularly with respect to the wrong-way responses that typically occur as transients (Buckley, 2005), as well as feed-forward behavior (Farquhar, 1978; Bunce, 1997; Franks et al., 1997; Tardieu and Simonneau, 1998; Ocheltree et al., 2014; compare with Mott and Peak, 2013). Although some of these models provide a pathway for incorporating the effect of ABA (Buckley, 2005), a lack of knowledge of ABA dynamics or action makes it difficult to integrate the influence of this active regulator of guard cell aperture into models. The stomatal behavior of single gene mutants (most notably the ABA synthesis and signaling mutants of Arabidopsis) strongly supports a role for ABA in mediating standard stomatal responses to changes in VPD. The stomata of these mutants are known to have less pronounced responses to a reduction in relative humidity compared with wild-type plants (Xie et al., 2006). Recently, molecular work has shown that guard cells express many of the genes required to synthesize ABA (Okamoto et al., 2009; Bauer et al., 2013), with molecular proxies for ABA level also indicating that the biochemical activity of ABA in the guard cell may increase following short-term exposure of leaves to a reduction in relative humidity (Waadt et al., 2014). These findings suggest a role for ABA in regulating stomatal responses to VPD and have led some to the conclusion that ABA synthesized autonomously by the guard cells is the predominant mechanism for stomatal responses to increased VPD (Bauer et al., 2013).Although the experimental evidence from molecular studies presents an argument for the role of ABA in the responses of stomata to changes in VPD, very few studies have quantified changes in ABA level in response to VPD. It is well established that ABA levels in leaves and guard cells can increase following the imposition of turgor loss or water stress (Pierce and Raschke, 1980; Harris et al., 1988; Harris and Outlaw, 1991). However, only a few studies have reported increases in foliar ABA level in response to high VPD (Bauerle et al., 2004; Giday et al., 2013), and none have investigated whether these observed dynamic changes or differences in ABA level were functionally relevant for stomatal control. In addition, no study has quantified the levels of ABA in guard cells during a transition in VPD.Here, we investigate the relative importance of ABA for the stomatal response to VPD in whole plants, sampled from across the vascular land plant lineage. We provide, to our knowledge, the first functional assessment of changes in ABA levels driving stomatal responses to VPD as well as critically investigate the recent suggestion that stomatal responses to VPD are driven by an autonomous guard cell synthesis of ABA. 相似文献
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Chun-Long Li Mei Wang Xiao-Meng Wu Dong-Hua Chen Hong-Jun Lv Jian-Lin Shen Zhu Qiao Wei Zhang 《Plant physiology》2016,170(2):1090-1104
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PYRABACTIN RESISTANCE1-LIKE8 Plays an Important Role for the Regulation of Abscisic Acid Signaling in Root 总被引:2,自引:0,他引:2
Regina Antoni Miguel Gonzalez-Guzman Lesia Rodriguez Marta Peirats-Llobet Gaston A. Pizzio Maria A. Fernandez Nancy De Winne Geert De Jaeger Daniela Dietrich Malcom J. Bennett Pedro L. Rodriguez 《Plant physiology》2013,161(2):931-941
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Sophie Hok Valérie Allasia Emilie Andrio Elodie Naessens Elsa Ribes Franck Panabières Agnès Attard Nicolas Ris Mathilde Clément Xavier Barlet Yves Marco Erwin Grill Ruth Eichmann Corina Weis Ralph Hückelhoven Alexandra Ammon Jutta Ludwig-Müller Lars M. Voll Harald Keller 《Plant physiology》2014,166(3):1506-1518
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Zhen-Yu Wang Chris Gehring Jianhua Zhu Feng-Min Li Jian-Kang Zhu Liming Xiong 《Plant physiology》2015,167(1):137-152
Osmotic stress activates the biosynthesis of the phytohormone abscisic acid (ABA) through a pathway that is rate limited by the carotenoid cleavage enzyme 9-cis-epoxycarotenoid dioxygenase (NCED). To understand the signal transduction mechanism underlying the activation of ABA biosynthesis, we performed a forward genetic screen to isolate mutants defective in osmotic stress regulation of the NCED3 gene. Here, we identified the Arabidopsis (Arabidopsis thaliana) Vacuolar Sorting Receptor1 (VSR1) as a unique regulator of ABA biosynthesis. The vsr1 mutant not only shows increased sensitivity to osmotic stress, but also is defective in the feedback regulation of ABA biosynthesis by ABA. Further analysis revealed that vacuolar trafficking mediated by VSR1 is required for osmotic stress-responsive ABA biosynthesis and osmotic stress tolerance. Moreover, under osmotic stress conditions, the membrane potential, calcium flux, and vacuolar pH changes in the vsr1 mutant differ from those in the wild type. Given that manipulation of the intracellular pH is sufficient to modulate the expression of ABA biosynthesis genes, including NCED3, and ABA accumulation, we propose that intracellular pH changes caused by osmotic stress may play a signaling role in regulating ABA biosynthesis and that this regulation is dependent on functional VSR1.Plant vacuoles are vital organelles for maintaining cell volume and cell turgor, regulating ion homeostasis and pH, disposing toxic materials, and storing and degrading unwanted proteins (Marty, 1999). To perform these diverse functions, vacuoles require an array of different and complex proteins. These proteins are synthesized at the endoplasmic reticulum (ER) and are transported to the vacuole through the vacuolar trafficking pathway. Perturbation of the vacuolar trafficking machinery affects many cellular processes, including tropisms, responses to pathogens, cytokinesis, hormone transport, and signal transduction (Surpin and Raikhel, 2004). The vacuolar trafficking system is comprised of several compartments: the ER, the Golgi apparatus, the trans-Golgi network (TGN), the prevacuolar compartment (PVC), and the vacuole. Vacuolar proteins synthesized at the ER are transported to the cis-Golgi via coat protein complex II (COPII) vesicles and are then transported to the TGN through the Golgi apparatus. In the TGN, proteins are sorted for delivery to their respective locations according to their targeting signal. Vacuolar proteins carrying a vacuolar sorting signal are thought to be recognized by vacuolar sorting receptors (VSRs), which are mainly located in the PVC, although sorting of vacuolar proteins may also occur at the ER and VSRs can be recycled from the TGN to the ER (Castelli and Vitale, 2005; Niemes et al., 2010). Multiple studies suggest that plant VSRs serve as sorting receptors both for lytic vacuole proteins (daSilva et al., 2005; Foresti et al., 2006; Kim et al., 2010) and for storage vacuole proteins (Shimada et al., 2003; Fuji et al., 2007; Zouhar et al., 2010).Osmotic stress is commonly associated with many environmental stresses, including drought, cold, and high soil salinity, that have a severe impact on the productivity of agricultural plants worldwide. Therefore, understanding how plants perceive and respond to osmotic stress is critical for improving plant resistance to abiotic stresses (Zhu, 2002; Fujita et al., 2013). It has long been recognized that osmotic stress can activate several signaling pathways that lead to changes in gene expression and metabolism. One important regulator of these signaling pathways is the phytohormone abscisic acid (ABA), which accumulates in response to osmotic stress. ABA regulates many critical processes, such as seed dormancy, stomatal movement, and adaptation to environmental stress (Finkelstein and Gibson, 2002; Xiong and Zhu, 2003; Cutler et al., 2010). De novo synthesis of ABA is of primary importance for increasing ABA levels in response to abiotic stress. ABA is synthesized through the cleavage of a C40 carotenoid originating from the 2-C-methyl-d-erythritol-4-phosphate pathway, followed by a conversion from zeaxanthin to violaxanthin catalyzed by the zeaxanthin epoxidase ABA1 and then to neoxanthin catalyzed by the neoxanthin synthase ABA4. Subsequently, a 9-cis-epoxycarotenoid dioxygenase (NCED) cleaves the violaxanthin and neoxanthin to xanthoxin. Xanthoxin, in turn, is oxidized by a short-chain alcohol dehydrogenase (ABA2) to abscisic aldehyde, which is converted to ABA by abscisic acid aldehyde oxidase3 (AAO3) using a molybdenum cofactor activated by the molybdenum cofactor sulfurase (ABA3; Nambara and Marion-Poll, 2005). In this pathway, it is generally thought that the cleavage step catalyzed by NCED is the rate-limiting step (Iuchi et al., 2000, 2001; Qin and Zeevaart, 2002; Xiong and Zhu, 2003). In Arabidopsis (Arabidopsis thaliana), five members of the NCED family (NCED2, NCED3, NCED5, NCED6, and NCED9) have been characterized (Tan et al., 2003). Of those, NCED3 has been suggested to play a crucial role in ABA biosynthesis, and its expression is induced by dehydration and osmotic stress (Iuchi et al., 2000, 2001; Qin and Zeevaart, 2002; Xiong and Zhu, 2003). Thus, understanding how the NCED3 gene is activated in response to osmotic stress is important for the elucidation of the mechanisms that govern plant acclimation to abiotic stress.We have used the firefly luciferase reporter gene driven by the stress-responsive NCED3 promoter to enable the genetic dissection of plant responses to osmotic stress (Wang et al., 2011). Here, we report the characterization of a unique regulator of ABA biosynthesis, 9-cis Epoxycarotenoid Dioxygenase Defective2 (CED2). The ced2 mutants are impaired in osmotic stress tolerance and are defective in the expression of genes required for ABA synthesis and consequently osmotic stress-induced ABA accumulation. The CED2 gene encodes VSR1, previously known to be involved in vacuolar trafficking but not known to be critical for osmotic stress induction of ABA biosynthesis and osmotic stress tolerance. Our study further suggests that intracellular pH changes might act as an early stress response signal triggering osmotic stress-activated ABA biosynthesis. 相似文献
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Reactive Oxygen Species-Dependent Nitric Oxide Production Contributes to Hydrogen-Promoted Stomatal Closure in Arabidopsis 总被引:2,自引:0,他引:2
Yanjie Xie Yu Mao Wei Zhang Diwen Lai Qingya Wang Wenbiao Shen 《Plant physiology》2014,165(2):759-773
The signaling role of hydrogen gas (H2) has attracted increasing attention from animals to plants. However, the physiological significance and molecular mechanism of H2 in drought tolerance are still largely unexplored. In this article, we report that abscisic acid (ABA) induced stomatal closure in Arabidopsis (Arabidopsis thaliana) by triggering intracellular signaling events involving H2, reactive oxygen species (ROS), nitric oxide (NO), and the guard cell outward-rectifying K+ channel (GORK). ABA elicited a rapid and sustained H2 release and production in Arabidopsis. Exogenous hydrogen-rich water (HRW) effectively led to an increase of intracellular H2 production, a reduction in the stomatal aperture, and enhanced drought tolerance. Subsequent results revealed that HRW stimulated significant inductions of NO and ROS synthesis associated with stomatal closure in the wild type, which were individually abolished in the nitric reductase mutant nitrate reductase1/2 (nia1/2) or the NADPH oxidase-deficient mutant rbohF (for respiratory burst oxidase homolog). Furthermore, we demonstrate that the HRW-promoted NO generation is dependent on ROS production. The rbohF mutant had impaired NO synthesis and stomatal closure in response to HRW, while these changes were rescued by exogenous application of NO. In addition, both HRW and hydrogen peroxide failed to induce NO production or stomatal closure in the nia1/2 mutant, while HRW-promoted ROS accumulation was not impaired. In the GORK-null mutant, stomatal closure induced by ABA, HRW, NO, or hydrogen peroxide was partially suppressed. Together, these results define a main branch of H2-regulated stomatal movement involved in the ABA signaling cascade in which RbohF-dependent ROS and nitric reductase-associated NO production, and subsequent GORK activation, were causally involved.Stomata are responsible for leaves of terrestrial plants taking in carbon dioxide for photosynthesis and likewise regulate how much water plants evaporate through the stomatal pores (Chaerle et al., 2005). When experiencing water-deficient conditions, surviving plants balance photosynthesis with controlling water loss through the stomatal pores, which relies on turgor changes by pairs of highly differentiated epidermal cells surrounding the stomatal pore, called the guard cells (Haworth et al., 2011; Loutfy et al., 2012).Besides the characterization of the significant roles of abscisic acid (ABA) in regulating stomatal movement, the key factors in guard cell signal transduction have been intensively investigated by performing forward and reverse genetics approaches. For example, both reactive oxygen species (ROS) and nitric oxide (NO) have been identified as vital intermediates in guard cell ABA signaling (Bright et al., 2006; Yan et al., 2007; Suzuki et al., 2011; Hao et al., 2012). The key ROS-producing enzymes in Arabidopsis (Arabidopsis thaliana) guard cells are the respiratory burst oxidase homologs (Rboh) D and F (Kwak et al., 2003; Bright et al., 2006; Mazars et al., 2010; Marino et al., 2012). Current available data suggest that there are at least two distinct pathways responsible for NO synthesis involved in ABA signaling in guard cells: the nitrite reductase (NR)- and l-Arg-dependent pathways (Desikan et al., 2002; Besson-Bard et al., 2008). Genetic evidence further demonstrated that removal of the major known sources of either ROS or NO significantly impairs ABA-induced stomatal closure. ABA fails to induce ROS production in the atrbohD/F double mutant (Kwak et al., 2003; Wang et al., 2012) and NO synthesis in the NR-deficient mutant nitrate reductase1/2 (nia1/2; Bright et al., 2006; Neill et al., 2008), both of which lead to impaired stomatal closure in Arabidopsis. Most importantly, ROS and NO, which function both synergistically and independently, have been established as ubiquitous signal transduction components to control a diverse range of physiological pathways in higher plants (Bright et al., 2006; Tossi et al., 2012).The guard cell outward-rectifying K+ channel (GORK) encodes the exclusive voltage-gated outwardly rectifying K+ channel protein, which was located in the guard cell membrane (Ache et al., 2000; Dreyer and Blatt, 2009). Expression profiles revealed that this gene is up-regulated upon the onset of drought, salinity, and cold stress and ABA exposure (Becker et al., 2003; Tran et al., 2013). Reverse genetic evidence further showed that GORK plays an important role in the control of stomatal movements and allows the plant to reduce transpirational water loss significantly (Hosy et al., 2003) and participates in the regulation of salinity tolerance by preventing salt-induced K+ loss (Jayakannan et al., 2013). Due to the high complexity of guard cell signaling cascades, whether and how ABA-triggered GORK up-regulation is attributed to the generation of cellular secondary messengers, such as ROS and NO, is less clear.Hydrogen gas (H2) was recently revealed as a signaling modulator with multiple biological functions in clinical trails (Ohsawa et al., 2007; Itoh et al., 2009; Ito et al., 2012). It was previously found that a hydrogenase system could generate H2 in bacteria and green algae (Meyer, 2007; Esquível et al., 2011). Although some earlier studies discovered the evolution of H2 in several higher plant species (Renwick et al., 1964; Torres et al., 1984), it was also proposed that the eukaryotic hydrogenase-like protein does not metabolize H2 (Cavazza et al., 2008; Mondy et al., 2014). Since the explosion limit of H2 gas is about 4% to 72.4% (v/v, in the air), the direct application of H2 gas in experiments is flammable and dangerous. Regardless of these problems to be resolved, the methodology, such as using exogenous hydrogen-rich water (HRW) or hydrogen-rich saline, which is safe, economical, and easily available, provides a valuable approach to investigate the physiological function of H2 in animal research and clinical trials. For example, hydrogen dissolved in Dulbecco’s modified Eagle’s medium was found to react with cytotoxic ROS and thus protect against oxidative damage in PC12 cells and rats (Ohsawa et al., 2007). The neuroprotective effect of H2-loaded eye drops on retinal ischemia-reperfusion injury was also reported (Oharazawa et al., 2010). In plants, corresponding results by using HRW combined with gas chromatography (GC) revealed that H2 could act as a novel beneficial gaseous molecule in plant responses against salinity (Xie et al., 2012; Xu et al., 2013), cadmium stress (Cui et al., 2013), and paraquat toxicity (Jin et al., 2013). More recently, the observation that HRW could delay the postharvest ripening and senescence of kiwifruit (Actinidia deliciosa) was reported (Hu et al., 2014).Considering the fact that the signaling cascades for salt, osmotic, and drought stresses share a common cascade in an ABA-dependent pathway, it would be noteworthy to identify whether and how H2 regulates the bioactivity of ABA-induced downstream components and, thereafter, biological responses, including stomatal closure and drought tolerance. To resolve these scientific questions, rbohD, rbohF, nia1/2, nitric oxide associated1 (noa1; Van Ree et al., 2011), nia1/2/noa1, and gork mutants were utilized to investigate the relationship among H2, ROS, NO, and GORK in the guard cell signal transduction network. By the combination of pharmacological and biochemical analyses with this genetics-based approach, we provide comprehensive evidence to show that H2 might be a newly identified bioeffective modulator involved in ABA signaling responsible for drought tolerance, that HRW-promoted stomatal closure was mainly attributed to the modulation of ROS-dependent NO generation, and that GORK might be the downstream target protein of H2 signaling. 相似文献
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