Phytophthora sojae Effector PsAvh113 Targets Transcription Factors in Nicotiana benthamiana

TL;DR

This study identifies how a pathogen effector from Phytophthora sojae interacts with plant transcription factors to enhance disease symptoms in Nicotiana benthamiana.

Contribution

The study reveals PsAvh113's interaction with specific transcription factors and its role in promoting disease resistance in plants.

Findings

PsAvh113 expression leads to 1769 differentially expressed genes in Nicotiana benthamiana.

Three transcription factors (NbNAC86, NbMyb4, and NbERF114) are significantly upregulated by PsAvh113.

Silencing these genes increases susceptibility to P. capsici, while overexpression enhances resistance.

Abstract

Phytophthora sojae is a type of pathogenic oomycete that causes Phytophthora root stem rot (PRSR), which can seriously affect the soybean yield and quality. To subvert immunity, P. sojae secretes a large quantity of effectors. However, the molecular mechanisms regulated by most P. sojae effectors, and their host targets remain unexplored. Previous studies have shown that the expression of PsAvh113, an effector secreted by Phytophthora sojae, enhances viral RNA accumulations and symptoms in Nicotiana benthamiana via VIVE assay. In this study, we analyzed RNA-sequencing data based on disease symptoms in N. benthamiana leaves that were either mocked or infiltrated with PVX carrying the empty vector (EV) and PsAvh113. We identified 1769 differentially expressed genes (DEGs) dependent on PsAvh113. Using stricter criteria screening and Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analysis of DEGs, we found that 38 genes were closely enriched in response to PsAvh113 expression. We selected three genes of N. benthamiana (NbNAC86, NbMyb4, and NbERF114) and found their transcriptional levels significantly upregulated in N. benthamiana infected with PVX carrying PsAvh113. Furthermore, individual silencing of these three genes promoted P. capsici infection, while their overexpression increased resistance to P. capsici in N. benthamiana. Our results show that PsAvh113 interacts with transcription factors NbMyb4 and NbERF114 in vivo. Collectively, these data may help us understand the pathogenic mechanism of effectors and manage PRSR in soybeans.

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