A transcription factor TOE3 simultaneously promotes growth and antiviral immunity by disrupting ABA core module in tobacco
TL;DR
It is found that the amino-terminal domain of TOE3 (T3N) inhibits abscisic acid (ABA) signaling, which reveals how TOE3 uncoupling to provide strategies for breeding crops with strong growth and antiviral immunity.
Abstract
Plant immune activation often reduces growth, which is defined as “growth-defense trade-off” (GDT). Uncoupling GDT is promising for breeding of elite cultivars with strong growth and immunity. We previously identified that AP2 transcription factor TARGET OF EARLY3 (TOE3) promotes both growth and antiviral defense. However, the mechanism underlying this GDT uncoupling remains unknown. Here, we find that the amino-terminal domain of TOE3 (T3N) inhibits abscisic acid (ABA) signaling. Mechanistically, T3N binds to an ABA receptor PYL4 to interfere with PYL4-PP2C4 interaction. The PYL4-PP2C4 module regulates tobacco growth and antiviral immunity. Thus, under normal conditions, T3N enhances tobacco growth via down-regulating ABA response. Upon TMV infection, the phosphorylation of T3N is induced. Phosphorylated T3N exhibits stronger binding affinity to PYL4 to further amplify its disruptive effect on PYL4-PP2C4 module and strongly block ABA response, thereby boosting antiviral immunity. These findings reveal how TOE3 uncouples GDT to provide strategies for breeding crops with strong growth and antiviral immunity.