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Updated: May 27, 2025

Assay for Pathogen-Associated Molecular Pattern PAMP-Triggered Immunity PTI in Plants
Published on: September 9, 2009
Puccinia striiformis Effector PNPi Suppresses TaIAA14 Expression to Inhibit Host Cell Death Response
Huiyutang Wang1, Xue Gao1, Yixi Kong1
1College of Agronomy and Biotechnology, Yunnan Agricultural University, Kunming, China.
Abstract:
Fungal pathogens secrete effectors that suppress the hypersensitive response (HR) of the host, characterised by programmed cell death, facilitating colonisation. However, how effectors manipulate host cell death remains poorly understood. In this study, we discovered that the Puccinia striiformis effector PNPi (Puccinia NPR1 interactor) suppressed BAX-induced cell death in Nicotiana benthamiana. This virulence was mediated by the FtsN domain of PNPi, and an enhanced suppression effect was observed when Ser129 was mutated into arginine. Further RNA-sequencing analysis revealed that auxin signalling was disturbed, with the auxin-responsive protein IAA29-like (NbIAA29) being downregulated during cell death suppression by PNPi. Exogenous application of auxins alleviated cell death suppression in N. benthamiana. Silencing NbIAA29 enhanced the PNPi-induced suppression; however, this effect was reduced in NbIAA29-silenced plants pretreated with auxins. Additionally, we confirmed the in vivo interaction between PNPi and TaIAA14, which is the homologous gene of NbIAA29 in wheat. Knocking down TaIAA14 through virus-induced gene silencing significantly increased the fungal development and reduced wheat cell death response. Overall, these results indicate that the P. striiformis effector PNPi suppresses the cell death response by targeting TaIAA14 to facilitate infection, advancing our understanding of how P. striiformis effectors manipulate host immunity and providing a theoretical basis for new strategies of sustainable disease control.
Insights
The Puccinia striiformis effector PNPi suppresses plant programmed cell death by targeting auxin signaling. This fungal virulence mechanism involves manipulating NbIAA29 in plants and TaIAA14 in wheat, aiding pathogen infection.
Area of Science:
- Plant Pathology
- Molecular Plant-Microbe Interactions
- Fungal Effector Biology
Background:
- Fungal pathogens secrete effectors to suppress host programmed cell death (hypersensitive response) for successful colonization.
- The precise mechanisms by which fungal effectors manipulate host cell death pathways are not fully understood.
Purpose of the Study:
- To investigate the role of the Puccinia striiformis effector PNPi in suppressing host cell death.
- To elucidate the molecular mechanisms underlying PNPi-mediated virulence and its interaction with host factors.
Main Methods:
- Functional analysis of the PNPi effector in Nicotiana benthamiana using BAX-induced cell death assays.
- RNA-sequencing to identify host genes affected by PNPi.
- Exogenous auxin application and gene silencing (NbIAA29) to assess auxin signaling involvement.
- In vivo interaction studies and virus-induced gene silencing (TaIAA14) in wheat.
Main Results:
- PNPi suppressed BAX-induced cell death in N. benthamiana, mediated by its FtsN domain.
- PNPi downregulated the auxin-responsive gene NbIAA29, and exogenous auxins partially restored cell death.
- PNPi interacted with wheat TaIAA14, and its knockdown enhanced fungal development and reduced wheat cell death.
Conclusions:
- The P. striiformis effector PNPi suppresses host cell death by targeting auxin signaling, specifically interacting with NbIAA29/TaIAA14.
- This effector-host interaction facilitates fungal infection and colonization.
- Findings provide insights into fungal virulence strategies and potential targets for disease control.
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