Hydrogen sulphide (H2 S) in the hidden half: Role in root growth, stress signalling and rhizospheric interactions.

Apart from nitric oxide (NO) and carbon monoxide (CO), hydrogen sulphide (H2 S) has emerged as a potential gasotransmitter that has regulatory roles in root differentiation, proliferation and stress signalling. H2 S metabolism in plants exhibits spatio-temporal differences that are intimately associated with sulphide signalling in the cytosol and other subcellular components, e.g. chloroplast and mitochondria. H2 S biosynthesis in plant organs uses both enzymatic and non-enzymatic pathways. H2 S generation in roots and aerial organs is modulated by developmental phase and changes in environmental stimuli. H2 S has an influential role in root development and in the nodulation process. Studies have revealed that H2 S is a part of the auxin and NO signalling pathways in roots, which induce lateral root formation. At the molecular level, exogenous application of H2 S regulates expression of several transcription factors, viz. LBD (Lateral organ Boundaries Domain), MYB (myeloblastosis) and AP2/ERF (Apetala 2/ Ethylene Response Factor), which stimulate upregulation of PpLBD16 (Lateral organ boundaries domain 16), thereby significantly increasing the number of lateral roots. Concomitantly, H2 S acts as a crucial signalling molecule in roots during various abiotic stresses, e.g. drought, salinity heavy metals (HMs), etc., and augments stress tolerance in plants. Interestingly, extensive crosstalk exists between H2 S, NO, ABA, calcium and ethylene during stress, which escalate plant defence and regulate plant growth and productivity. Hence, the present review will elaborate the role of H2 S in root development, stress alleviation, legume-Rhizobium symbiosis and rhizosphere signalling. The review also examines the mechanism of H2 S-mediated abiotic stress mitigation and cross-talk with other signaling molecules.

Melatonin and calcium function synergistically to promote the resilience through ROS metabolism under arsenic-induced stress.

The interplay between melatonin (Mel) and calcium (Ca2+) in enhancing tolerance to metalloid toxicity and underlying physiological and biochemical mechanisms of this relationship still remains unknown. The present study reveals that the signaling molecules Mel and/or Ca2+ enhanced tolerance of Vicia faba (cv. Tara) plant to metalloid arsenic (As) toxicity. However, a combination of Mel and Ca2+ was more efficient than alone. Plants grew with As exhibited enhanced hydrogen peroxide, superoxide anion, electrolyte leakage, lipid peroxidation together with increased reactive oxygen species (ROS) producing enzymes, such as NADPH oxidase and glycolate oxidase (GOX). On the contrary, an inhibition in chlorophyll (Chl) biosynthesis and gas exchange parameters (net photosynthetic rate, stomatal conductance, intercellular carbon dioxide concentration) was observed. Under As toxicity conditions, the application of Mel and Ca2+ synergistically suppressed the plants' program cell death features (nucleus condensation and nucleus fragmentation) in guard cells of stomata, DNA damage, and formation of ROS in guard cells, leaves and roots. Moreover, it enhanced gas exchange parameters and activity of enzymes involved in photosynthesis process (carbonic anhydrase and RuBisco), Chl biosynthesis (δ-aminolevulinic acid dehydratase), and decreased activity of Chl degrading enzyme (chlorophyllase) under As toxicity conditions. Our investigation evidently established that expression of ATP synthase, Ca2+-ATPase, Ca2+-DPKase, Hsp17.6 and Hsp40 was found maximum in the plants treated with Mel + Ca2+, resulting in higher tolerance of plants to As stress. Also, increased total soluble carbohydrates, cysteine, and Pro accumulation with increased Pro synthesizing enzyme (Δ1-pyrroline-5-carboxylate synthetase (P5CS) and decreased Pro degrading enzyme (proline dehydrogenase) in Mel + Ca2+ treated plants conferred As toxicity tolerance. The obtained results postulate strong evidence that the application of Mel along with Ca2+ enhances resilience against As toxicity by upregulating the activity of plasma membrane H+-ATPase, enzymes involved in antioxidant system, and ascorbate-glutathione pathway.