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

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 1.0 mM 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.