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 Ser(129) 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.