Calcium-hydrogen sulfide crosstalk during K-deficient NaCl stress operates through regulation of Na/H antiport and antioxidative defense system in mung bean roots.

Present investigation reports the role of calcium (Ca) and hydrogen sulfide (HS) crosstalk associated with Vigna radiata seedlings subjected to K deficient conditions under short-term (24 h) and long-term (72 h) NaCl stress. Perusal of the data reveals that under short-term NaCl stress an initial decline in K level led to the elevation in Ca and HS levels along with improvement in antioxidant system and reduction in reactive oxygen species (ROS) production. Under long-term NaCl stress a further decline in K content was deleterious that led to a lower K/Na ratio. This was followed by reduction in antioxidant system along with excessive accumulation of ROS and methylglyoxal content, and increased membrane damage. However, supplementation of the seedling roots with Ca enhanced biosynthesis of HS through enhancing cysteine pool. The present findings suggest that synergistic action of Ca and HS induced the activity of H-ATPase that created H gradient which in turn induced Na/H antiport system that accelerated K influx and Na efflux. All of these together contributed to a higher K/Na ratio, activation of antioxidative defense system, and maintenance of redox homeostasis and membrane integrity in Ca-supplemented stressed seedlings. Role of Ca and HS in the regulation of Na/H antiport system was validated by the use of sodium orthovanadate (plasma membrane H-ATPase inhibitor), tetraethylammonium chloride (K channel blocker), and amiloride (Na/H antiporter inhibitor). Application of Ca-chelator EGTA (ethylene glycol-bis(b-aminoethylether)-N,N,N',N'-tetraacetic acid) and HS scavenger hypotaurine abolished the effect of Ca, suggesting the involvement of Ca and HS in the alleviation of NaCl stress. Moreover, use of EGTA and HT also substantiates the downstream functioning of HS during Ca-mediated regulation of plant adaptive responses to NaCl stress. To sum up, present findings reveal the association of Ca and HS signaling in the regulation of ion homeostasis and antioxidant defense during K-deficient NaCl stress.