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Chen, J.; Khan, M.S.S.; Islam, F.; Ye, Y.; , .; Zhao, B.; Fu, Z. Crosstalk of H2S with Signaling/Phytohormones under Changing Environments. Encyclopedia. Available online: https://encyclopedia.pub/entry/22079 (accessed on 11 July 2025).
Chen J, Khan MSS, Islam F, Ye Y,  , Zhao B, et al. Crosstalk of H2S with Signaling/Phytohormones under Changing Environments. Encyclopedia. Available at: https://encyclopedia.pub/entry/22079. Accessed July 11, 2025.
Chen, Jian, Muhammad Saad Shoaib Khan, Faisal Islam, Yajin Ye,  , Biying Zhao, Zhengqing Fu. "Crosstalk of H2S with Signaling/Phytohormones under Changing Environments" Encyclopedia, https://encyclopedia.pub/entry/22079 (accessed July 11, 2025).
Chen, J., Khan, M.S.S., Islam, F., Ye, Y., , ., Zhao, B., & Fu, Z. (2022, April 21). Crosstalk of H2S with Signaling/Phytohormones under Changing Environments. In Encyclopedia. https://encyclopedia.pub/entry/22079
Chen, Jian, et al. "Crosstalk of H2S with Signaling/Phytohormones under Changing Environments." Encyclopedia. Web. 21 April, 2022.
Crosstalk of H2S with Signaling/Phytohormones under Changing Environments
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This entry is adapted from the peer-reviewed paper 10.3390/ijms23084272

Hydrogen sulfide (H2S) serves as an important gaseous signaling molecule that is involved in intra- and intercellular signal transduction in plant–environment interactions. In plants, H2S is formed in sulfate/cysteine reduction pathways. The activation of endogenous H2S and its exogenous application has been found to be highly effective in ameliorating a wide variety of stress conditions in plants. The H2S interferes with the cellular redox regulatory network and prevents the degradation of proteins from oxidative stress via post-translational modifications (PTMs). H2S-mediated persulfidation allows the rapid response of proteins in signaling networks to environmental stimuli. In addition, regulatory crosstalk of H2S with other gaseous signals and plant growth regulators enable the activation of multiple signaling cascades that drive cellular adaptation.

hydrogen sulfide biotic stress abiotic stress salicylic acid abscisic acid jasmonic acid ethylene auxin phytohormones

1. Crosstalk of H2S and Abscisic Acid (ABA)

Plants modify ABA levels continually in response to changing physiological and environmental conditions, while bioactive ABA levels are sustained through a fine balance between generation and catabolism [1][2][3]. Several ABA receptors are involved in signal perception and transduction [1]. Earlier studies revealed that the interaction of H2S with ABA receptor genes implied that H2S regulates ABA signaling via influencing ABA receptors [1][4][5]. H2S application in drought-stressed plants upregulated the expression of potential ABA receptors such as RCAR (The regulatory component of ABA), ABAR (abscisic acid receptor), PYR1 (pyrabactin resistant protein), GTG1 (GPCR-type G proteins), and CHLH (H subunit of the Mg-chelatase) [1][6]. Some studies point out that ABA regulates many physiological processes, and H2S sometimes regulates these responses in a similar way [1][7][6]. Exogenous application of ABA triggers the endogenous production of H2S, suggesting complex crosstalk between two signaling molecules exists under drought stress conditions [1]. Similarly, under heat stress, ABA could trigger the accumulation of endogenous H2S and act as a new downstream gaseous signaling molecule that regulates ABA-induced stress responses in heat-stressed plants [1].
In plants, stomatal closure or opening is regulated by guard cells. The plant hormone ABA regulates the function of several ion channels in an ABA-dependent manner to control stomatal closure and opening [6][8][9][10][11]. A wealth of literature provides ample evidence that H2S regulates stomatal aperture in various plant species, and it may have implications for ABA-dependent stomatal closures in plants under stressful conditions [6]. The earlier study of Wang et al. [12] illuminated this underlying mechanism and revealed that exogenous application of H2S activates the S-type anion currents in guard cells of Arabidopsis. Concurrently, the elevated level of free Ca2+ is a prerequisite for its activation [12]. H2S triggers Ca2+ waves in guard cells. In guard cells, Ca2+ sensing is perceived by a heterotrimeric G-protein β-subunit (AGB1) that collaborates in Ca2+ induced stomatal closure in Arabidopsis [13]. Ca2+ ions also activate SLAC1 by stimulating CPK (calcium-dependent protein kinase) activity. It was observed that lower concentrations of ABA partially impaired stomatal closure in CPK quadruple mutant plants; however, higher concentrations of ABA effectively close stomata. The application of Ca2+ chelator (1,2-bis(o-aminophenoxy) ethane-N,N,N,N-tetraacetic acid (BAPTA) completely inhibited the ABA-mediated activation of anion channel in guard cells and prevented the ABA-induced stomatal closure [14][15]. These studies showed that H2S and ABA are signaling components in stomatal closure in plants.
A recent study demonstrated that H2S mediated persulfidation of SnRK2.6/OST1 in response to ABA signaling initiated stomatal closure (Figure 1). In guard cells, SnRK2.6/OST1 acts as a core component of ABA signaling that controls stomatal movements, and its function is tightly regulated by H2S-mediated PTMs. Under certain physiological conditions, ABA induces the generation of H2S by activating DES1 in the guard cell. The accumulation of H2S persulfidates SnRK2.6 on Cyc131 and Cys137, which are close to the catalytic loop and near to Ser175 residues, which is vital for the phosphorylation of SnRK2.6 [16][17][18][19][20]. The Cys137 can also undergo S-nitrosylation and could inhibit the activity of SnRK2.6 [21][19]. However, persulfidation promotes SnRK2.6 activity, and it is believed that persulfidation occurs earlier than S-nitrosylation [21][20]. Due to Cyc131/137 persulfidation induced changes, Ser175 affinity for ATP-γ-phosphate proton acceptor site (Asp140) increases, which leads to the robust autophosphorylation of Ser175 and triggers efficient interaction of SnRK2.6 with its target. This observation confirms that H2S-mediated persulfidation positively impacts the function of SnRK2.6 in ABA-mediated stomatal closure in guard cells [21][18]. Likewise, Shen et al. [22] reported that during drought stress, ABA signaling in guard cells is promoted by H2S interaction with ABA. The drought stress mediates the accumulation of ABA, which stimulates persulfidation of DES1 in a redox-dependent manner. At the physiological level, enhanced accumulation of H2S in the guard cell leads to the persulfidation of H2O2 producing enzymes, such as NADPH oxidase, which triggers the generation of H2O2 in the guard cell that reinforces ABA signaling and the closure of stomata [22]. Another study revealed that abscisic acid insensitive 4 (ABI4) is involved in the facilitation of ABA and H2S crosstalk at the transcriptional level (Figure 1). ABI4 is a vital TF in the ABA signaling cascade, and little was known about the PTMs that regulate its activity in response to ABA/H2S interaction in plants. The ABA accumulation triggers a massive generation of H2S that leads to the persulfidation of ABI4, which allows the binding of ABI4 to the E1 motif of the MAPKKK18 (mitogen-activated protein kinase kinase kinase 18) promoter to activate DES1 transcription to close stomata under the ABA-dependent signaling cascade [23]. This research provides compelling evidence that the DES1/H2S-ABI4 module acts downstream of ABA signaling to regulate stomatal closure [23][24] (Figure 1).
/media/item_content/202204/626ba8c5d7555ijms-23-04272-g004.png
Figure 1. Under normal conditions, ABA receptors (PYR/PYL/RCAR) bind to the PP2Cs and inhibit the activity of SnRK2.6, which deactivates NADPH oxidase, SALC1, and other ion channels to reinforce the normal functioning of stomata. Under water-stressed conditions, ABA signaling stimulates ABA receptors (PYR/PYL/RCAR) that lead to the activation of SnRK2.6, which triggers SLAC1 and NADPH oxidase to produce H2O2 and regulate stomatal movements. During drought stress, ABA signaling increases the biosynthesis of H2S via persulfidation of ABI4-mediated activation of DES1 transcription. The burst of H2S in guard cells activates the S-type anion and spikes the Ca2+ wave alongside strong persulfidation of SnRK2.6. The persulfidated SnRK2.6 robustly phosphorylates SALAC1 and NADPH oxidase to produce a long-lasting burst of ROS to modulate water efflux in guard cells to close stomata, similarly to the way that ABA induces stomatal closure.
In some of the recently published reports, it was also revealed that H2S might be involved in the biosynthesis of ABA in guard cells [25]. The H2S promotes the synthesis of cysteine, which is a substrate of ABA3 (molybdenum cofactor sulfurase) enzymes that regulate the activation of AAO3 (abscisic aldehyde oxidase 3) [26]. The higher accumulation of cysteine stimulates the activity of AAO (in vivo) and favors the synthesis of ABA [27] by stimulating the transcript abundance of NCED3 (9-cis-epoxycarotenoid dioxygenase 3). It was revealed that H2S could boost ABA synthesis, because in a cysteine-biosynthesis-depleted mutant with the disrupted ABA biosynthesis, the H2S was unable to induce stomatal closure [18][19]. All these studies point out the involvement/crosstalk of H2S with SnRK2.6, CPK6, MAPKKK18, ABI1, NADPH oxidase, Ca2+, and ROS in ABA-mediated signaling for stomatal movements in plants [18][19][20].

2. Nitric Oxide (NO) and H2S: Two Interacting Gaseous Molecules Essential for Plant Functioning

Nitric oxide (NO) is also a lipophilic gaseous hormone that could diffuse into inter- or intra cellular spaces without the need for any carrier or transport channel. NO is also involved in PTMs via tyrosine nitration, metal nitrosylation, and S-nitrosylation, whereas H2S mediated-PTM is associated with persulfidation. However, all these reactions led to the modification of structure, localization, and function of target proteins. Several studies have shown that H2S interacts with NO and other signaling molecules to modulate plant development and stress responses [28][29][30][31][32]. Earlier reports indicate that the interaction of H2S towards NO is complementary or inhibitory [33][34][35][36][37]. The positive or negative interaction of these two gaseous signaling molecules may be dependent upon the dosage of exogenous H2S or NO application. For instance, the level of NO was reduced in plant tissues that were treated with H2S modulator (NaSH) [9][38]. However, crosstalk of NO-H2S showed synergistic interaction during abiotic stresses and inhibition of ethylene-induced fruit ripening, whereas antagonistic interaction of H2S-NO-ethylene is also reported [39][40][41][42]. The discrepancy in H2S and NO interaction may depend upon the specific location of these gaseous molecules in the cell that deicide their signaling behavior [43]. There is also a possibility that both gaseous molecules may compete for the same targeting protein in the cell. For example, SnRK2.6 is a target of both NO and H2S biomolecules, and S-nitrosylation of SnRK2.6 via NO inhibits its activity while persulfidation enhances its activity and mediate stomatal movements [18][20]. Additionally, H2S and NO could react among themselves to produce nitrosothiol compounds that are also involved in signaling responses. The crosstalk of ROS with H2S–NO cascades also modulates their interactions in positive or negative ways [44]. Taken together, the nature of the interaction between NO and H2S may vary for different physiological functions based upon their location and concentration in the cell.
NO and H2S belong to the family of reactive nitrogen and sulfur species (RNS and RSS), and their positive combinations regulate various important physiological and molecular processes in plants. For example, the interaction of H2S with NO and Ca2+ regulate lateral root (LR) formation in tomato plants. The exogenous application of NO triggers the accumulation of H2S in tomato roots due to the upregulation of H2S biosynthesis enzymes, which induce later root formation [45]. However, when H2S inhibitor/scavengers were applied, LRs’ formation was partially arrested. These findings indicate that NO-induced H2S synthesis governs the later root formation [45][46].
Stomatal movements are regulated by many endogenous signaling molecules; among them, H2S and NO crosstalk are also responsible for stomatal closure. In a recent study, with the employment of pharmacological, spectrophotographic, and fluorescence microscope techniques, the coordinated action of H2S and NO in the presence of 2,4-epibrassinolide (EBR) was involved in stomatal regulation [47][48]. The authors demonstrated the application of EBR-induced stomatal closure in a dose and time-dependent manner via modifying the levels of NO, and H2S in Vicia faba. The application of EBR upregulated the activity of L-/D-cysteine desulfhydrase and enhanced the endogenous levels of H2S together with H2O2 and NO generation in guard cells. The application of the H2S inhibitor significantly reduced L-/D-cysteine desulfhydrase activity and H2S endogenous production, which in turn abolished the EBR mediated stomatal closure effect [47]. The H2S scavengers/inhibitors did not affect the NO and H2O2 levels in guard cells. However, the application of NO and H2O2 inhibitors/modulators significantly affected the endogenous production of H2S and its biosynthesis enzymes and compromised the EBR-induced stomatal closure [47]. Similarly, Jing et al. [49] found that H2S may function downstream of NO in ethylene-induced stomatal closure in V. faba. These results indicate that H2S and NO participate in EBR-mediated stomatal closure response and H2S signifies an essential constituent downstream of H2O2 and NO in EBR-induced stomatal closure in V. faba [47][50]. Previous studies demonstrated that H2S inhibits ABA-mediated NO generation in Arabidopsis and Capsicum annuum guard cells. Conversely, H2S increased NO levels in alfalfa seedlings [33][38], while H2S induces NO generation in Arabidopsis guard cells. Conversely, NO scavenger inhibited H2S-induced stomatal closure [36]. However, investigation of H2S-mediated guard cell signaling in Arabidopsis revealed that the H2S induced signaling cascade for stomatal closure is NO-dependent [11], and both H2S and NO equally contribute to the production of 8-mercapto-cGMP, which triggers stomatal closure. In the same way, H2S and NO collaborate in ethylene induce stomatal closure responses in Arabidopsis plants, and H2S generation is mediated by NO, which suggests that H2S acts as a downstream signaling agent in ethylene induce stomatal closure [51].
The crosstalk of H2S and NO in the alleviation of metal toxicity is also reported, but these studies focused more on stress physiology and lacked underlying molecular mechanisms of crosstalk [52]. The exogenous application of H2S donor alleviated Cd stress in alfalfa plants by triggering the synthesis of NO. The interaction mechanism between H2S and NO improved the Cd stress tolerance by reducing Cd accumulation and lowering the lipid peroxidation in stressed plants [19]. Another study, where H2S and NO scavenger and inhibitor were applied to Cd stressed bermudagrass plants, revealed that depletion of NO makes them more vulnerable to metal toxicity. Furthermore, through pharmacological experiments, it was demonstrated that NO-activated H2S was essential for cadmium stress responses in bermudagrass [53]. In Pisum sativum, positive interaction of NO and H2S was also explored under arsenate stress [54]. The application of H2S donor triggered endogenous H2S and NO accumulation in P. sativum, which led to the strengthening of the antioxidant defense system, reduced arsenate accumulation, and maintained the redox balance of P. sativum plant under metal toxicity [54]. Similarly, the crosstalk of NO and H2S reduced oxidative stress and increased salinity tolerance in alfalfa, while barley seedlings under H2S application regulate ion homeostasis under salinity via maintaining the NO signaling pathway [55][37]. Most of the published studies on the interaction of NO and H2S in the context of metal toxicity/salinity proposed that crosstalk of these gaseous molecules ameliorates stress-induced toxicity in exposed plants via (i) improving the antioxidant defense to prevent oxidative stress, (ii) reducing the metal uptake, and (iii) by modulating the expression of associated metal transporter genes [52].
In short, H2S and NO are both gaseous biomolecules with common signaling pathways, and it seems that one pathway controls the functions of the other [52]. The persulfidation promoted by H2S reacts with thiol groups in the same way as NO does in modification through S-nitrosation [52][56]. However, there is still a need to investigate the interaction of H2S and NO in different plant species, tissues, and diverse environmental conditions to unveil the regulatory mechanism of the NO–H2S signaling cascade in plants.

3. H2S-Mediated Manipulation of Auxin Signaling in Plants

The development of roots, including lateral and adventitious roots, is incredibly important for normal plant growth and the successful completion of the life cycle. Plant root architecture is mainly based on the LR that is generated from pericycle founder cells [48]. The plant hormone auxin and environmental factors (i.e., water and nutrient availability) are key influencers in lateral root formation [57][58]. Since auxin is a master regulator of root development in plants, there have always been complex crosstalks of auxin with other signaling agents in the root development [57][59][60].
Several studies have reported that H2S and auxin interact with each other to regulate root growth; however, mechanistic insight remains to be elucidated [61][47][62]. The earlier studies demonstrated that the application of exogenous H2S on the sweet potato seedling stimulated the numbers and length of adventitious roots by modulating the IAA levels in a dose-dependent manner [47]. It was also noted that pretreatment of H2S donor upregulated the transcript abundance of the auxin-dependent Cyclin-Dependent Kinases gene (CDKA1) and a cell cycle regulatory gene (CYCA2) [46][60]. The activity of both of these genes was inhibited either by auxin blocker or H2S inhibitor, which illustrated that H2S mediated LR development is dependent upon the IAA signaling via influencing the regulation of CDKA1 and CYCA2 [46][60]. Similarly, when higher doses of H2S donor (1 mM) were applied, the RBOH1 (respiration burst oxidase homologous) transcript was significantly upregulated and ROS accumulation triggered the later root formation [63] (Figure 2). The pharmacological studies revealed that H2S triggered the expression activity of RBOH1, which stimulated an H2O2-mediated increase in IAA signaling via regulation of CDKA1, CYCA2, and Kip-Related Protein 2 (KRP2), to activate LR formation [63]. A transcriptomic study revealed that exogenous application of H2S impacted the regulation of various auxin pathway-related genes. The accumulation of auxin biosynthesis genes (TAA1 and UGT74B1) was correlated with the increase in auxin levels in roots. The genes involved in auxin polar subcellular distribution, such as PIN2, ABCB1, ABCB19, PILS3, and PILS7, were differentially expressed, while PIN1c appeared as a hub gene on the basis of WGCNA analysis. This research provides sufficient evidence that H2S induced root development emanates from regulating the genes involved in transcriptional control and synthesis of auxin [62] (Figure 2).
/media/item_content/202204/626ba8f7b2938ijms-23-04272-g005.png
Figure 2. Schematic representation of the signaling pathways involving auxin, DES (cysteine desulfhydrase), NO (Nitric oxide), and hydrogen sulfide (H2S) interaction during lateral root formation in plants. The interaction between H2S and NO under the influence of auxin participates in the development of the lateral root via modulating the expressions and activities of different effector genes or proteins in a framework of regulatory pathways to permit root growth. miRNA: Micro RNA; ARFs: Auxin Response Factors; CDKA1: Cyclin-Dependent Kinases gene; CYCA2: cell cycle regulatory gene; KRP2: Kip-Related Protein 2; NR: Nitrate reductase; LR: lateral root.
In some studies, the application of higher dosages of H2S showed changes in root development and inhibition of auxin transport due to the alteration in the polar subcellular distribution of the PIN proteins [62]. The polar subcellular movement of auxin in root cells is an actin-dependent process, and H2S is involved in the regulation of actin dynamics due to the persulfidation and depolymerization of F actin [64]. Furthermore, during root hair development, the H2S fine-tuned polar auxin transport via persulfidation and actin filament growth [64][65]. In the root developmental process, actin-binding proteins work downstream of the H2S signal transduction pathway because actin-binding proteins are involved in the depolymerization of F-actin in root cells, which regulate the distribution and transport of auxin [65]. Auxin affects the patterning and organization of the actin cytoskeleton in root cells during cellular growth [66][67]. Conversely, the actin cytoskeleton modulates the directional transport of auxin by altering auxin efflux carriers [68][69]. This finding indicates that overproduction of H2S significantly increases the S-sulfhydration level of actin-2 and decreases the distribution of actin cytoskeleton in root cells, thereby reducing auxin’s polar transport, which restricts the LR and the root hair growth [70][64][65].
The exposure of plants to CH4 strongly induces H2S production and affects the root growth, adventitious root numbers, and root length in cucumber explants [71][72]. At the transcriptional level, it was observed that H2S modulated auxin-signaling genes (Aux22D-like and Aux22B-like) reinforce the CH4-induced cucumber adventitious rooting network [73][72][74][75]. Similarly, in tomato plants, LRs formation was also triggered by the CH4-mediated H2S signaling cascade. It was hypothesized that the possible involvement of auxin transport and auxin signaling in CH4-induced LR formation is involved [76]. However, more biochemical and genetic investigations are required to analyze the detailed targets and their functions in root organogenesis under CH4-H2S-Auxin crosstalks [72][76].
The signaling pathways of H2S and auxin interaction under the chilling stress were recently explored in cucumber plants [77][78][79] (Figure 3). The research demonstrated that chilling stress in cucumber arrested photosynthesis and induced oxidative stress; however, deleterious effects were alleviated due to exogenous application of H2S donor or IAA application [79]. The expression of YUCCA2 (auxin biosynthesis gene) and auxin contents were very high in chilling-exposed cucumber seedlings. This result may be due to the inhibition of polar transport of IAA in long-term chilling stress, which increases auxin concentration in leaves and inhibits plant growth. The complex interaction of H2S and IAA under chilling stress improved the activities and gene expression of key enzymes of the Calvin–Benson cycle (Ribulose-1,5-bisphosphatecarboxylase, fructose bisphosphatase, sedoheptulose-1,7-bisphosphatase, fructose-1,6-bisphosphate aldolase, and transketolase) and strengthened the photosynthetic carbon assimilation capacity [79] (Figure 6). The results also indicated that auxin is a downstream signal for the protective effects induced by H2S under chilling-induced tolerance in cucumber plants [79]. Furthermore, the overexpression of auxin response factor 5 (ARF5) in cucumber unveiled the molecular mechanism of cold tolerance. In transgenic plants overexpressing ARF5 under cold stress, ARF5 directly activates the expression of dehydration-responsive element-binding protein 3 (DREB3) for the reinforcement of auxin signaling to improve cold stress tolerance in cucumber in response to H2S application [80] (Figure 3). Previously, it was observed that auxin response factors (ARFs) and miR390 formed an auxin-responsive regulatory network (miR390-TAS3-ARF2/ARF3/ARF4) that strengthens auxin signaling in plants [81].
/media/item_content/202204/626ba9273b73eijms-23-04272-g006.png
Figure 3. A regulatory model elucidates the role of hydrogen sulfide (H2S) in mediating the cold stress response in plants via auxin signaling. In the presence of cold stress, the phospholipase D (PLD) is activated and degrades the phosphatidylcholine (PC) phospholipid of the cell membrane. As a result, phosphatidic acid (PA) is produced, which further regulates protein phosphatase 2A (PP2A), nitrate reductase (NR), nitric oxide (NO), and finally H2S. In the absence of H2S, auxin distribution, photosynthesis, and carbon assimilation are inhibited in plants under exposure to cold stress. The exogenous application or endogenous H2S mediate auxin redistribution in plants and activate the antioxidant defense system along with improved photosynthesis to restore the normal function of the plant at physiological levels. On the other hand, C-repeat binding factors (CBFs) and ARF (auxin-responsive proteins) promote the dehydration-responsive element-binding (DREB) and other related proteins to promote cold tolerance at molecular levels under H2S-mediated signaling.

4. Interaction between H2S and Gibberellic Acid

Gibberellic acid (GA) is a phytohormone that substantially influences the seed germination and growth of seedlings. Imbibition of barley grains in 0.25 mM NaHS solution caused an upsurge in antioxidant enzymes such as CAT, POD, APX, and SOD in the aleurone layer [82]. In tomato plants, boron stress reduced dry weight, photosynthetic rate, water content, chlorophyll content, and increased H2O2, MDA, and endogenous H2S. GA foliar spray reduced the harmful effects of boron by raising endogenous H2S, Ca2+, and K+, as well as lowering the levels of H2O2, MDA, and boron, as well as membrane leakage. Surprisingly, NaHS further increased GA-induced boron tolerance, whereas H2S scavengers prevented it (HT). These findings indicate that H2S plays a signaling role downstream of GA in the development of boron stress tolerance in tomato plants. During cadmium stress, the NaHS treatment stimulated the activities of amylase and antioxidant enzymes in cucumber hypocotyls and radicles, which might be connected to H2S-induced Cd stress tolerance.
Moreover, GA can cause programmed cell death (PCD); however, NaHS application can prevent PCD by lowering L-cysteine desulfhydrase (LCD) activity and accumulating endogenous H2S in wheat aleurone layers [83]. GA-induced PCD is reduced in the aleurone layer in the NaHS-treated seeds by diminishing the endogenous GSH levels. H2S concentration regulates the GSH levels, which upsurges expression of the HEME OXYGENASE-1 (HO-1) gene, resulting in the alleviation of apoptosis in the aleurone layer and an overall decrease in PCD. Hence, in the aleurone layer, there are regulatory interactions between GA, H2S, GSH, and HO-1. Intriguingly, NaHS pretreatment slowed Arabidopsis seed germination, but Arabidopsis des1 mutant seedlings were more susceptible to ABA than the wild-type. These findings suggest that H2S interacts with GA in plants to control seed germination under normal and stressful circumstances.

5. Interaction between H2S and Melatonin

Melatonin (N-acetyl-5-methoxytryptamine) is a multifaceted phytohormone involved in germination, ripening, flowering, photosynthesis, and defense mechanisms [84]. In plants, melatonin alters the permeability of the cell layer governed by ion transporters, which control stomatal opening and closure. Studies have shown that melatonin can increase the photosynthetic capacity of plants, which leads to greater levels of nitrogen and chlorophyll. In tomato and wheat, increased transcription of stress-responsive genes was induced by melatonin, resulting in better tolerance to high temperature [85][86]. Furthermore, melatonin cross-talks with various plant hormones and signaling molecules. It was also discovered that H2S and melatonin conjointly helped alleviate salt stress-induced growth reduction in tomatoes, and exogenous melatonin treatment assisted in regulating early H2S signaling [87]. In wheat, the heat stress-induced oxidative damage was mitigated by exogenous melatonin and further increased the H2S production, suggesting that melatonin-mediated H2S was involved in alleviating the oxidative stress. However, the melatonin function was attenuated when H2S was inhibited by its inhibitor, indicating that the cross-talk between H2S and melatonin, and possibly melatonin, regulates heat stress signaling by acting upstream of H2S [88].

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Subjects: Plant Sciences
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Jian Chen
,
Muhammad Saad Shoaib Khan
,
Faisal Islam
,
Yajin Ye
,
,
Biying Zhao
,
Zhengqing Fu
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