Dual function of GbNAC2 in flavonoid metabolism and hormonal pathways enhances salt tolerance in Ginkgo biloba

TL;DR

This study shows how the GbNAC2 gene helps ginkgo plants tolerate salt by boosting flavonoid production and hormonal signaling.

Contribution

GbNAC2 is shown to uniquely mediate crosstalk between flavonoid and hormonal pathways to enhance salt tolerance in ginkgo.

Findings

GbNAC2 overexpression increases root length by over 60% and flavonoid content by more than 20% in transgenic ginkgo.

Transcriptome analysis reveals GbNAC2 upregulates genes in auxin biosynthesis and flavonoid synthesis pathways.

GbNAC2 binds the GbAREB3 promoter to enhance ABA signaling, improving salt resilience when combined with exogenous ABA.

Abstract

NAC transcription factors are central regulators of plant salt tolerance, yet their specific roles in ginkgo salt response remain unclear. Here, GbNAC2 was identified as a salinity-induced transcriptional activator in ginkgo, orchestrating two key adaptive responses. GbNAC2 overexpression significantly improved salt tolerance in transgenic plants, accompanied by over 60% increase in root length, and more than 20% increase in flavonoid content compared to wild type (WT). Transcriptome analysis of GbNAC2-overexpressing ginkgo calli revealed that genes related to auxin biosynthesis, and those involved in the flavonoid synthesis pathway, were significantly upregulated in transgenic calli. Mechanistically, GbNAC2 directly binds the GbAREB3 promoter to enhance ABA signaling, and exogenous ABA treatment further enhances salt resilience. The present findings unveil a unique crosstalk mediated by GbNAC2 between flavonoid-antioxidant systems and auxin-ABA hormonal networks, effectively resolving the growth-defense trade-off under salinity in ginkgo.

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