Interactions between hydrogen sulphide and nitric oxide regulate two soybean citrate transporters during the alleviation of aluminium toxicity.

Hydrogen sulphide (H S) is emerging as an important signalling molecule involved in plant resistance to various stresses. However, the underlying mechanism of H S in aluminium (Al) resistance and the crosstalk between H S and nitric oxide (NO) in Al stress signalling remain elusive. Citrate secretion is a wide-spread strategy for plants against Al toxicity. Here, two citrate transporter genes, GmMATE13 and GmMATE47, were identified and characterized in soybean. Functional analysis in Xenopus oocytes and transgenic Arabidopsis showed that GmMATE13 and GmMATE47 mediated citrate exudation and enhanced Al resistance. Al treatment triggered H S generation and citrate exudation in soybean roots. Pretreatment with an H S donor significantly elevated Al-induced citrate exudation, reduced Al accumulation in root tips, and alleviated Al-induced inhibition of root elongation, whereas application of an H S scavenger elicited the opposite effect. Furthermore, H S and NO mediated Al-induced GmMATE expression and plasma membrane (PM) H -ATPase activity and expression. Further investigation showed that NO induced H S production by regulating the key enzymes involved in biosynthesis and degradation of H S. These findings indicate that H S acts downstream of NO in mediating Al-induced citrate secretion through the upregulation of PM H -ATPase-coupled citrate transporter cotransport systems, thereby conferring plant resistance to Al toxicity.