Auxin acts as a downstream signaling molecule involved in hydrogen sulfide-induced chilling tolerance in cucumber.

Abstract

This report proves a cross talk between H2S and IAA in cold stress response, which has presented strong evidence that IAA acts as a downstream signal mediating the H2S-induced stress tolerance in cucumber seedlings. We evaluated changes in endogenous hydrogen sulfide (H2S) and indole-3-acetic acid (IAA) emission systems, and the interactive effect of exogenous H2S and IAA on chilling tolerance in cucumber seedlings. The results showed that chilling stress increased the activity and relative mRNA expression of L-/D-cysteine desulfhydrase (L-/D-CD), which in turn induced the accumulation of endogenous H2S. Similarly, the endogenous IAA system was triggered by chilling stress. We found that 1.0mM sodium hydrosulfide (NaHS, an H2S donor) significantly enhanced the activity of flavin monooxygenase (FMO) and relative expression of FMO-like proteins (YUCCA2), which in turn elevated endogenous IAA levels in cucumber seedlings. However, IAA had little effects on activities of L-/D-CD and endogenous H2S levels. H2S-induced IAA production accompanied by increase in chilling tolerance, as shown by the decrease in stress-induced electrolyte leakage (EL) and reactive oxygen species (ROS) accumulation, and increase in gene expressions and enzyme activities of photosynthesis. 1-naphthylphthalamic acid (NPA, an IAA polar transport inhibitor) declined H2S-induced chilling tolerance and defense genes' expression. However, scavenging of H2S had a little effect on IAA-induced chilling tolerance. These results suggest that IAA acting as a downstream signaling molecule is involved in the H2S-induced chilling tolerance in cucumber seedlings.