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Peer-reviewedCC BY-NCPlant biotechnology journal

The Cytosolic Iron-Sulfur Cluster Assembly Targeting Complex Is Hijacked by Magnaporthe Effector AvrPi9 to Suppress Rice Resistance.

  • Huanbin Shi1
  • Zhiquan Liu1
  • Ying Zhang1
  • Runjing Li1
  • Zhizhen Fu1
  • Ya Chen1
  • Hui Wen1
  • Liang Cai1
  • Zhengting Chen1
  • Jiehua Qiu1
  • Yanjun Kou1
  1. 1State Key Laboratory of Rice Biology and Breeding, China National Rice Research Institute, Hangzhou, China.
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Abstract

The cytosolic iron-sulfur (Fe-S) cluster assembly (CIA) targeting complex mediates the maturation of cytosolic and nuclear Fe-S proteins and governs core eukaryotic cellular processes. However, whether this complex contributes to plant disease resistance remains unclear. Here, we show that the Magnaporthe oryzae avirulence effector AvrPi9 targets the host CIA targeting complex to suppress rice blast resistance. AvrPi9 physically interacts with and stabilizes OsAE7, a core subunit of the CIA targeting complex. Using biochemical and genetic approaches, we demonstrate that OsAE7 facilitates Fe-S protein maturation, including the Fe-S protein aconitase OsACO1, and negatively regulates blast resistance in cooperation with another CIA targeting complex subunit, OsCIA1, and the carrier protein OsNAR1 in rice. Furthermore, ectopic expression of AvrPi9 enhances the activity of the CIA complex and the maturation of OsACO1. Knockout of OsACO1 elevates ferrous iron levels, triggers a reactive oxygen species (ROS) burst, and activates pathogenesis-related gene transcription, thereby strengthening rice resistance to blast. Our findings reveal a critical role of the CIA targeting complex in plant disease resistance and uncover a novel virulence strategy whereby AvrPi9 hijacks the host CIA pathway to dampen basal resistance and promote infection.

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Cite

BibTeXRIS
BibTeX
@article{shi2026cytosolic,
  title = {{The Cytosolic Iron-Sulfur Cluster Assembly Targeting Complex Is Hijacked by Magnaporthe Effector AvrPi9 to Suppress Rice Resistance.}},
  author = {Huanbin Shi and Zhiquan Liu and Ying Zhang and Runjing Li and Zhizhen Fu and Ya Chen and Hui Wen and Liang Cai and Zhengting Chen and Jiehua Qiu and Yanjun Kou},
  journal = {Plant biotechnology journal},
  year = {2026},
  month = oct,
  doi = {10.1111/pbi.70773},
  url = {https://europepmc.org/article/MED/42904532},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - The Cytosolic Iron-Sulfur Cluster Assembly Targeting Complex Is Hijacked by Magnaporthe Effector AvrPi9 to Suppress Rice Resistance.
AU  - Huanbin Shi
AU  - Zhiquan Liu
AU  - Ying Zhang
AU  - Runjing Li
AU  - Zhizhen Fu
AU  - Ya Chen
AU  - Hui Wen
AU  - Liang Cai
AU  - Zhengting Chen
AU  - Jiehua Qiu
AU  - Yanjun Kou
PY  - 2026
DA  - 2026/10/21
JO  - Plant biotechnology journal
DO  - 10.1111/pbi.70773
UR  - https://europepmc.org/article/MED/42904532
AB  - The cytosolic iron-sulfur (Fe-S) cluster assembly (CIA) targeting complex mediates the maturation of cytosolic and nuclear Fe-S proteins and governs core eukaryotic cellular processes. However, whether this complex contributes to plant disease resistance remains unclear. Here, we show that the Magnaporthe oryzae avirulence effector AvrPi9 targets the host CIA targeting complex to suppress rice blast resistance. AvrPi9 physically interacts with and stabilizes OsAE7, a core subunit of the CIA targeting complex. Using biochemical and genetic approaches, we demonstrate that OsAE7 facilitates Fe-S protein maturation, including the Fe-S protein aconitase OsACO1, and negatively regulates blast resistance in cooperation with another CIA targeting complex subunit, OsCIA1, and the carrier protein OsNAR1 in rice. Furthermore, ectopic expression of AvrPi9 enhances the activity of the CIA complex and the maturation of OsACO1. Knockout of OsACO1 elevates ferrous iron levels, triggers a reactive oxygen species (ROS) burst, and activates pathogenesis-related gene transcription, thereby strengthening rice resistance to blast. Our findings reveal a critical role of the CIA targeting complex in plant disease resistance and uncover a novel virulence strategy whereby AvrPi9 hijacks the host CIA pathway to dampen basal resistance and promote infection.
SN  - 1467-7644
SN  - 1467-7652
ER  -