PL06 Gasotransmitters in plant signalling: An exciting new field is emerging

Abstract

Gaseous molecules are nowadays well established signalling components transmitting inter and intracellular information. Gasotransmitters are synthesized and metabolized by specific enzymatic activities, they possess specific cellular targets and regulate a number of physiological responses directed to keep cellular homeostasis in a changing environment. While typical messenger molecules amplify signal cascades, gasotransmitters can act through chemical modification of specific protein targets resulting in a rapid influence on cellular metabolism. In the last decade, findings describing the nitric oxide (NO) functions in plant cell signalling were a breakthrough in plant biology [1] , [2] . Recently, hydrogen sulfide (H2S) has emerged as a critical player in plant physiology acting as NO partner in some cases but within a yet unknown and unexplored scenario [3] , [4] . Plants control the gas exchange with the environment through the regulation of the stomatal pore formed by two specialized cells named guard cells. The size of the stomatal pore is finely regulated by volume changes of the guard cells, driven by the influx and efflux of osmotically active solutes through plasma membrane (PM) ion channels. Abscisic acid (ABA) is the master phytohormone controlling stomatal closure under water deficit conditions. We have demonstrated that ABA induces increases in NO concentration in guard cells [5] . NO, in turn, inactivates inward rectifying K+ K in + channels by increasing cytosolic Ca2+ concentrations [6] contributing to the net loss of solutes from guard cells required for stomatal closure. We have found that the gasotransmitter H2S induces the stomatal closure through a NO-mediated pathway [7] . The mutants of the plant model Arabidopsis are usually used as genetical tools for unravelling gene functions. Stomata of the Arabidopsis mutant atdes1 defective in l -cysteine desulfhydrase (DES), one of the enzymes responsible of H2S synthesis, do not respond to ABA treatment, indicating that H2S is required for ABA-mediated stomatal closure. The Arabidopsis mutant abi1 is impaired in ABA signalling and insensitive to H2S, suggesting that a functional ABA signalling is critical for H2S effect in guard cells. Thus, data support a connection between H2S and NO to operate a fine regulation of gas exchange resulting in a control of plant water status. Experiments are in progress to find experimentally H2S targets among the guard cell PM ion channels. The richness of the redox chemistry of the different NO forms (NO, NO− and NO+) reacting with H2S (H+ and HS−) in guard cells is an intriguing puzzle to decipher ABA crosstalk with NO and H2S. To understand the redox regulation of guard cells in different plant environmental scenarios is necessary to unveil how the physiology of guard cells makes use of NO and H2S as intermediates leading to selective PM ion channels activation/inhibition.