PeMPK7 enhances poplar salt tolerance by coordinating phytohormone dynamics and activating an ethylene-ERF114 regulatory module

Salt stress constrains poplar growth. The mitogen-activated protein kinase (MAPK) cascade and phytohormones are key regulators of plant salt tolerance. However, the mechanisms by which MAPK cascades orchestrate hormone homeostasis under salt stress in poplar are still poorly understood. This study shows that overexpressing PeMPK7 improved poplar salt tolerance. After 12 h of NaCl treatment, salicylic acid and abscisic acid (ABA) contents in PeMPK7 -overexpressing poplars were significantly higher than in wild-type plants ( P < 0.05). Transcriptomic profiling revealed that PeMPK7 reprogrammed phytohormone metabolism and signaling pathways, notably up-regulating ethylene (ET) biosynthesis genes ( ACS1 , ACO1 ) together with genes associated with indole-3-acetic acid, cytokinin, ABA, gibberellic acid, and jasmonic acid. Weighted gene co-expression network analysis suggested that PeMPK7 may act upstream of NAC072 , NAC002 , and TGA7 , which are associated with ABA metabolism and signaling under salt stress. Among differentially expressed transcription factor genes, PagERF114 expression was induced by salt in PeMPK7 -overexpressing plants and could be boosted by exogenous ET. Transgenic poplars overexpressing PagERF114 displayed enhanced salt tolerance, lower MDA content, and higher SOD/POD activities, demonstrating that PagERF114 enhances salt tolerance. Taken together, our findings suggest that PeMPK7 fine-tunes phytohormone homeostasis and partially enhances salt tolerance through an ethylene-associated pathway involving PagERF114 . • PeMPK7 overexpression confers enhanced salt tolerance in poplar. • Salt-induced ABA/SA surge while high IAA/GA1 retention under non-stress in PeMPK7 -OE poplar. • PeMPK7 rewires salt-responsive ET, IAA, CK, ABA, GA, and JA pathways. • PeMPK7 acts on 14 ABA hubs and NAC072 / NAC002 / TGA7 to regulate salt-induced ABA signaling. • PeMPK7 confers poplar salt tolerance through the ET- ERF114 module by reducing oxidative damage.