The phytohormone abscisic acid (ABA) plays pivotal roles in triggering stomatal closure and facilitating adaptation of plants to drought stress. Hydrogen sulfide (H 2 S), a small signaling gas molecule, is involved in ABA-dependent stomatal closure. However, how H 2 S regulates ABA signaling remains largely unclear.Here, we show that ABA induces the production of H 2 S catalyzed by L-CYSTEINE DESULFHYDRASE1 (DES1) in guard cells, and H 2 S in turn positively regulates ABA signaling through persulfidation of Open Stomata 1 (OST1)/SNF1-RELATED PROTEIN KINASE2.6 (SnRK2.6). Two cysteine (Cys) sites, Cys131 and Cys137, which are exposed on the surface of SnRK2.6 and close to the activation loop, were identified to be persulfidated, which promotes the activity of SnRK2.6 and its interaction with ABA response element-binding factor 2 (ABF2), a transcription factor acting downstream of ABA signaling. When Cys131, Cys137, or both residues in SnRK2.6 were substituted with serine (S), H 2 S-induced SnRK2.6 activity and SnRK2.6-ABF2 interaction were partially (SnRK2.6 C131S and SnRK2.6 C137S ) or completely (SnRK2.6 C131SC137S ) compromised. Introduction of SnRK2.6 C131S , SnRK2.6 C137S , or SnRK2.6 C131SC137S into the ost1-3 mutant could not rescue the mutant phenotype: less sensitivity to ABA-and H 2 S-induced stomatal closure and Ca 2+ influx as well as increased water loss and decreased drought tolerance. Taken together, our study reveals a novel post-translational regulatory mechanism of ABA signaling whereby H 2 S persulfidates SnRK2.6 to promote ABA signaling and ABA-induced stomatal closure.
Phototaxis is characteristic of the pelagic larval stage of most bottom-dwelling marine invertebrates. Larval phototaxis is mediated by simple eyes that can express various types of light-sensitive G-protein-coupled receptors known as opsins. Since opsins diversified early during metazoan evolution in the marine environment, understanding underwater light detection could elucidate this diversification. Opsins have been classified into three major families, the r-opsins, the c-opsins, and the Go/RGR opsins, a family uniting Go-opsins, retinochromes, RGR opsins, and neuropsins. The Go-opsins form an ancient and poorly characterized group retained only in marine invertebrate genomes. Here, we characterize a Go-opsin from the marine annelid Platynereis dumerilii. We found Go-opsin1 coexpressed with two r-opsins in depolarizing rhabdomeric photoreceptor cells in the pigmented eyes of Platynereis larvae. We purified recombinant Go-opsin1 and found that it absorbs in the blue-cyan range of the light spectrum. To characterize the function of Go-opsin1, we generated a Go-opsin1 knockout Platynereis line by zinc-finger-nuclease-mediated genome engineering. Go-opsin1 knockout larvae were phototactic but showed reduced efficiency of phototaxis to wavelengths matching the in vitro Go-opsin1 spectrum. Our results highlight spectral tuning of phototaxis as a potential mechanism contributing to opsin diversity.
A number of recent studies identified hydrogen sulfide (H2S) as an important signal in plant development and adaptation to environmental stress. H2S has been proven to participate in ethylene-induced stomatal closure, but how the signaling pathways of H2S and ethylene interact is still unclear. Here, we reveal how H2S controls the feedback-regulation of ethylene biosynthesis in tomato (Solanum lycopersicum) under osmotic stress. We found that ethylene induced the production of H2S in guard cells. The supply of hypotaurine (HT; a H2S scavenger) or DL-pro-pargylglycine (PAG; a synthetic inhibitor of H2S) removed the effect of ethylene or osmotic stress on stomatal closure. This suggests that ethylene-induced H2S is a downstream component of osmotic stress signaling, which is required for ethylene-induced stomatal closure under osmotic stress. We further found that H2S inhibited ethylene synthesis through inhibiting the activity of 1-aminocyclopropane-1-carboxylic acid (ACC) oxidases (ACOs) by persulfidation. A modified biotin-switch method (MBST) showed that H2S can induce persulfidation of LeACO1 and LeACO2 in a dose-dependent manner, and that persulfidation inhibits the activity of LeACO1 and LeACO2. We also found that LeACO1 is persulfidated at cysteine 60. These data suggested that ethylene-induced H2S negatively regulates ethylene biosynthesis by persulfidation of LeACOs. In addition, H2S was also found to inhibit the expression of LeACO genes. The results provide insight on the general mode of action of H2S and contribute to a better understanding of a plant’s response to osmotic stress.
Ciliary and rhabdomeric photoreceptor cells represent two main lines of photoreceptor-cell evolution in animals. The two cell types coexist in some animals, however how these cells functionally integrate is unknown. We used connectomics to map synaptic paths between ciliary and rhabdomeric photoreceptors in the planktonic larva of the annelid Platynereis and found that ciliary photoreceptors are presynaptic to the rhabdomeric circuit. The behaviors mediated by the ciliary and rhabdomeric cells also interact hierarchically. The ciliary photoreceptors are UV-sensitive and mediate downward swimming in non-directional UV light, a behavior absent in ciliary-opsin knockout larvae. UV avoidance overrides positive phototaxis mediated by the rhabdomeric eyes such that vertical swimming direction is determined by the ratio of blue/UV light. Since this ratio increases with depth, Platynereis larvae may use it as a depth gauge during vertical migration. Our results revealed a functional integration of ciliary and rhabdomeric photoreceptor cells in a zooplankton larva.
Hydrogen sulfide (H2S) and hydrogen peroxide (H2O2) function as the signaling molecules in plants responding to salt stresses. The present study presents a signaling network involving H2S and H2O2 in salt resistance pathway of the Arabidopsis root. Arabidopsis roots were sensitive to 100 mM NaCl treatment, which displayed a great increase in electrolyte leakage (EL) and Na(+)/K(+) ratio under salt stress. The treatment of H2S donors sodium hydrosulfide (NaHS) enhanced the salt tolerance by maintaining a lower Na(+)/K(+) ratio. In addition, the inhibition of root growth under salt stress was removed by H2S. Further studies indicated that H2O2 was involved in H2S-induced salt tolerance pathway. H2S induced the production of the endogenous H2O2 via regulating the activities of glucose-6-phosphate dehydrogenase (G6PDH) and plasma membrane (PM) NADPH oxidase, with the treatment with dimethylthiourea (DMTU, an ROS scavenger), diphenylene iodonium (DPI, a PM NADPH oxidase inhibitor), or glycerol (G6PDH inhibitor) removing the effect of H2S. Treatment with amiloride (an inhibitor of PM Na(+)/H(+) antiporter) and vanadate (an inhibitor of PM H(+)-ATPase) also inhibited the activity of H2S on Na(+)/K(+) ratio. Through an analysis of quantitative real-time polymerase chain reaction and Western blot, we found that H2S promoted the genes expression and the phosphorylation level of PM H(+)-ATPase and Na(+)/H(+) antiporter protein level. However, when the endogenous H2O2 level was inhibited by DPI or DMTU, the effect of H2S on the PM Na(+)/H(+) antiporter system was removed. Taken together, H2S maintains ion homeostasis in the H2O2-dependent manner in salt-stress Arabidopsis root.
Cadmium (Cd 2+ ) is a common toxic heavy metal ion. We investigated the roles of hydrogen sulfide (H 2 S) and cysteine (Cys) in plant responses to Cd 2+ stress. The expression of H 2 S synthetic genes LCD and DES1 were induced by Cd 2+ within 3 h, and endogenous H 2 S was then rapidly released. H 2 S promoted the expression of Cys synthesis-related genes SAT1 and OASA1, which led to endogenous Cys accumulation. The H 2 S and Cys cycle system was stimulated by Cd 2+ stress, and it maintained high levels in plant cells. H 2 S inhibited the ROS burst by inducing alternative respiration capacity (AP) and antioxidase activity. H 2 S weakened Cd 2+ toxicity by inducing the metallothionein (MTs) genes expression. Cys promoted GSH accumulation and inhibited the ROS burst, and GSH induced the expression of phytochelatin (PCs) genes, counteracting Cd 2+ toxicity. In summary, the H 2 S and Cys cycle system played a key role in plant responses to Cd 2+ stress. The Cd 2+ tolerance was weakened when the cycle system was blocked in lcddes1-1 and oasa1 mutants. This paper is the first to describe the role of the H 2 S and Cys cycle system in Cd 2+ stress and to explore the relevant and specificity mechanisms of H 2 S and Cys in mediating Cd 2+ stress.Cadmium (Cd 2+ ) is a common toxic heavy metal ion in the environment. It greatly affects the growth and development of plants and is harmful to human health through the food chain 1,2 . Because of its carcinogenic properties and its detrimental effects on the growth of organisms, Cd 2+ contamination of agricultural soil has become a critical concern. Preventing reduced growth and accumulation of Cd 2+ in harvested organs of plants growing on Cd 2+ -contaminated soils has become an urgent task as it can contribute to food safety. Thus, it is important to explore plant stress defense mechanisms and to find ways to reduce the Cd 2+ accumulation in grains.As a heavy metal not participating in redox reactions, Cd 2+ can easily dissolve in water and quickly be taken up by plant roots 3,4 . The physiological consequences of Cd 2+ toxicity in plants are chlorosis, stunted growth, and cell death, among others [5][6][7] . At the cellular level, Cd 2+ can alter protein structure and inhibit enzyme activity by binding to sulfhydryl and carbonyl groups and replacing essential co-factors of enzymes [7][8][9] . The overproduction of reactive oxygen species (ROS) is the primary response of plants to Cd 2+ with negative impact on cell function 10 . Further damage can be caused by ROS-independent, secondary mechanisms. Lipid peroxidation is the most deleterious effect caused by Cd 2+ -induced ROS 4 . Malondialdehyde (MDA), one of the decomposition products of lipid peroxidation, can modify active substrates in plant cells, including nucleic acids, proteins and saccharides 11 . To become resistant to Cd 2+ toxicity, plants have developed several strategies, such as inducing the
Hydrogen sulfide (H2S) signaling has been considered a key regulator of plant developmental processes and defenses. In this study, we demonstrate that high levels of H2S inhibit auxin transport and lead to alterations in root system development. H2S inhibits auxin transport by altering the polar subcellular distribution of PIN proteins. The vesicle trafficking and distribution of the PIN proteins are an actin-dependent process. H2S changes the expression of several actin-binding proteins (ABPs) and decreases the occupancy percentage of F-actin bundles in the Arabidopsis roots. We observed the effects of H2S on F-actin in T-DNA insertion mutants of cpa, cpb and prf3, indicating that the effects of H2S on F-actin are partially removed in the mutant plants. Thus, these data imply that the ABPs act as downstream effectors of the H2S signal and thereby regulate the assembly and depolymerization of F-actin in root cells. Taken together, our data suggest that the existence of a tightly regulated intertwined signaling network between auxin, H2S and actin that controls root system development. In the proposed process, H2S plays an important role in modulating auxin transport by an actin-dependent method, which results in alterations in root development in Arabidopsis.
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