# The AP-1 Sigma Subunit Gene PsAP1 Acts as a Key Pathogenicity Factor by Regulating Metabolic Reprogramming in Puccinia striiformis f. sp. tritici

## TL;DR

This study identifies a gene in wheat stripe rust fungus that helps it infect plants by altering plant metabolism and suppressing immunity.

## Contribution

The study reveals PsAP1 as a novel pathogenicity factor in rust fungi through metabolic reprogramming and immune suppression.

## Key findings

- PsAP1 expression is highly induced during early infection stages in Puccinia striiformis f. sp. tritici.
- Silencing PsAP1 in wheat reduced pathogen growth, sporulation, and biomass by over 60%.
- PsAP1 disrupts host pathways like MAPK signaling, glutathione, and carbohydrate metabolism.

## Abstract

Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), poses a severe threat to global wheat production. The adaptor protein complex AP-1 plays a crucial role in vesicular trafficking, yet its function in rust fungi remains poorly understood. In this study, a gene encoding an AP-1 σ subunit, designated PsAP1, was identified in Pst. The expression of PsAP1 was highly induced during the early infection stage. Heterologous expression of PsAP1 in a Fusarium graminearum mutant partially restored its pathogenic defects. Subcellular localization analysis revealed that PsAP1 localizes to the plasma membrane, cytoplasm, and nucleus. Silencing PsAP1 in wheat using Barley stripe mosaic virus-mediated host-induced gene silencing (BSMV-HIGS) significantly attenuated Pst pathogenicity, reducing hyphal growth by 6.7% (colony diameter), sporulation by 61.6% (lesion length), and pathogen biomass by 66%, along with enhanced accumulation of host reactive oxygen species. Transcriptomic analysis further demonstrated that silencing PsAP1 disrupted multiple pathways, including MAPK signaling, glutathione metabolism, and carbohydrate metabolism. These findings indicate that PsAP1 facilitates Pst infection by modulating vesicular trafficking, suppressing host immunity, and reprogramming host metabolism. This study provides novel insights into the pathogenic mechanisms of rust fungi and suggests a potential target for disease control.