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<p>PHYTOCHROME INTERACTING FACTOR 4 (PIF4) is known as a basic helix-loop-helix (bHLH) transcription factor that interacts with phytochrome and is integral to the Phytochrome B (phyB)-mediated regulation of seedling de-etiolation and photomorphogenesis, primarily by modulating cell expansion. Previous research has indicated that auxin might exacerbate pathogen-induced diseases by suppressing salicylic acid (SA)-dependent host defense mechanisms or through pathways independent of SA. This study was conducted to elucidate the function of PIF4 in orchestrating plant growth and innate immunity. Experiments with a PIF4 loss-of-function mutant revealed heightened immune defense against type III secretion system (T3SS) deficient bacteria <i>Pseudomonas syringae pv. tomato</i> (<i>Pto hrcC</i><sup><i>−</i></sup>), suggesting that PIF4 suppresses immunity. Upon pathogen detection, PIF4 upregulated the expression of indole acetic acid (IAA) biosynthesis-related genes, thereby promoting plant growth, while concurrently downregulating genes essential for SA biosynthesis, which are critical for PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Furthermore, PIF4 attenuated flg22-induced reactive oxygen species (ROS) production and callose accumulation. Moreover, the hypersensitive response and ROS production induced by <i>Pto</i> effectors <i>AvrRpm1</i> and <i>AvrRpt2</i> were diminished in the <i>pif4-1</i> mutant, reinforcing the notion that PIF4 negatively influences ETI. Therefore, these findings revealed that PIF4 exhibited a negative function in plant innate defense signaling during dynamic interactions between <i>Arabidopsis</i> and <i>Pseudomonas</i>.</p>

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PIF4 Negatively Regulates Plant Defense Against Pseudomonas syringae via Suppression of PAMP- and Effector-Triggered Immunity

  • 期刊论文

  • 发表日期：

    2025年11月12日

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  • Donah Mary Macoy,
  • Shahab Uddin,
  • Kris John Silvano,
  • Gyeong Ryul Ryu,
  • Hamad Khan,
  • Rakhimov Abdurakhim Ramazon Ugli,
  • Gyeongik Ahn,
  • Joon-Yung Cha,
  • Woe-Yeon Kim,
  • Min Gab Kim

摘要

PHYTOCHROME INTERACTING FACTOR 4 (PIF4) is known as a basic helix-loop-helix (bHLH) transcription factor that interacts with phytochrome and is integral to the Phytochrome B (phyB)-mediated regulation of seedling de-etiolation and photomorphogenesis, primarily by modulating cell expansion. Previous research has indicated that auxin might exacerbate pathogen-induced diseases by suppressing salicylic acid (SA)-dependent host defense mechanisms or through pathways independent of SA. This study was conducted to elucidate the function of PIF4 in orchestrating plant growth and innate immunity. Experiments with a PIF4 loss-of-function mutant revealed heightened immune defense against type III secretion system (T3SS) deficient bacteria Pseudomonas syringae pv. tomato (Pto hrcC−), suggesting that PIF4 suppresses immunity. Upon pathogen detection, PIF4 upregulated the expression of indole acetic acid (IAA) biosynthesis-related genes, thereby promoting plant growth, while concurrently downregulating genes essential for SA biosynthesis, which are critical for PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Furthermore, PIF4 attenuated flg22-induced reactive oxygen species (ROS) production and callose accumulation. Moreover, the hypersensitive response and ROS production induced by Pto effectors AvrRpm1 and AvrRpt2 were diminished in the pif4-1 mutant, reinforcing the notion that PIF4 negatively influences ETI. Therefore, these findings revealed that PIF4 exhibited a negative function in plant innate defense signaling during dynamic interactions between Arabidopsis and Pseudomonas.