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Author

Jiale Jiang

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Open access Aug 2026

The Small GTPase RHO1 Regulates ROS Homeostasis and Differentially Responds to Pathogens Infection via Interaction With Aquaporin TIP1;1 in Nicotiana

ABSTRACT Small G‐proteins are crucial regulators in plant growth and environmental responses. However, the mechanistic basis underlying their regulation of plant immunity to different pathogens is still poorly understood. Here, we showed that the small GTPase Ras homologous 1 (RHO1) responded differently to infection by distinct pathogens. Overexpression of RHO1 increased the plant susceptibility to chilli veinal mottle virus (ChiVMV) and necrotrophic Botrytis cinerea infections but enhanced plant resistance to the biotrophic bacterium Pseudomonas syringae . Further exploration revealed that there existed a direct interaction between RHO1 and tonoplast intrinsic protein 1;1 (TIP1;1), an aquaporin involved in water movement and the transport of hydrogen peroxide (H2O2) between vacuoles and cytoplasm. Under pathogen infection, the interaction between RHO1 and TIP1;1 could affect the distribution of reactive oxygen species (ROS) in the cytoplasm and vacuoles, promote the accumulation of ROS in the cytoplasm, leading to different responses of plant cells to pathogens with different lifestyles. Furthermore, the expression level of TIP1;1 was altered under infection by different pathogens. Our results demonstrate a mechanism by which the small GTPase RHO1 regulates ROS compartmentalization to affect the plant response to different pathogen infections, indicating the diversity of responses of a plant gene to different biotic factors.

Bo-Wen Yuan, Chenglong Ji, Bolei Jiao et al. · 0 citations
Open access Aug 2026

A transcription factor TOE3 simultaneously promotes growth and antiviral immunity by disrupting ABA core module in tobacco

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.

Bolei Jiao, Baijun Wu, H. Fang et al. · 0 citations