GmWRKY31 and GmHDL56 Enhances Resistance to Phytophthora sojae by Regulating Defense-Related Gene Expression in Soybean.

Sujie Fan,Pengfei Xu,Fanshan Meng,Shuzhen Zhang,Lidong Dong,Rongpeng Li,Qun Cheng,Dan Han,Wencheng Lu,Liangyu Jiang,Junjiang Wu,Feng Zhang

doi:10.3389/fpls.2017.00781

Abstract

Phytophthora root and stem rot of soybean [Glycine max (L.) Merr.] caused by the oomycete Phytophthora sojae, is a destructive disease worldwide. The molecular mechanism of the soybean response to P. sojae is largely unclear. We report a novel WRKY transcription factor (TF) in soybean, GmWRKY31, in the host response to P. sojae. Overexpression and RNA interference analysis demonstrated that GmWRKY31 enhanced resistance to P. sojae in transgenic soybean plants. GmWRKY31 was targeted to the nucleus, where it bound to the W-box and acted as an activator of gene transcription. Moreover, we determined that GmWRKY31 physically interacted with GmHDL56, which improved resistance to P. sojae in transgenic soybean roots. GmWRKY31 and GmHDL56 shared a common target GmNPR1 which was induced by P. sojae. Overexpression and RNA interference analysis demonstrated that GmNPR1 enhanced resistance to P. sojae in transgenic soybean plants. Several pathogenesis-related (PR) genes were constitutively activated, including GmPR1a, GmPR2, GmPR3, GmPR4, GmPR5a, and GmPR10, in soybean plants overexpressing GmNPR1 transcripts. By contrast, the induction of PR genes was compromised in transgenic GmNPR1-RNAi lines. Taken together, these findings suggested that the interaction between GmWRKY31 and GmHDL56 enhances resistance to P. sojae by regulating defense-related gene expression in soybean.

Highlights

Phytophthora root and stem rot (PRR), which is caused by the oomycete Phytophthora sojae, is one of the most destructive diseases of soybean [Glycine max (L.) Merr.] and is responsible for $1–2 billion losses per year worldwide (Tyler, 2007)
GmWRKY31 expression was significantly induced by P. sojae, and the accumulation of GmWRKY31 mRNA reached a peak at 24 h under P. sojae stress, followed by a decline (Supplementary Figure S2B)
The lesion area of the GmNPR1-OE lines was significantly (P < 0.01) smaller and the lesion area of the GmNPR1-RNA interference (RNAi) lines was larger than that of wild-type plants (WT) after 5 days infection with P. sojae (Figure 7F). These results indicate that the overexpression of GmNPR1 in soybean plants improved resistance to P. sojae, whereas susceptibility to P. sojae was enhanced in GmNPR1-RNAi transgenic soybean plants

Summary

Introduction

Phytophthora root and stem rot (PRR), which is caused by the oomycete Phytophthora sojae, is one of the most destructive diseases of soybean [Glycine max (L.) Merr.] and is responsible for $1–2 billion losses per year worldwide (Tyler, 2007). Resistant cultivars carrying major resistance (R) genes against P. sojae (Rps genes) have been a cornerstone for the management of the pathogen for 50 years (Schmitthenner, 1985; Buzzell and Anderson, 1992). Rps gene resistance is race-specific, qualitatively inherited and confers an immune type of response to infection by P. sojae. This qualitative resistance tends to be shortlived because R-genes are neutralized by adaptation of P. sojae populations (Schmitthenner, 1985). GmWRKY27 inhibits the expression of the downstream gene GmNAC29 by binding to the W-boxes in the promoter region of GmNAC29, leading to abiotic stress tolerance (Wang F. et al, 2015), and OsWRKY6 binds directly to WLE1 and W-boxes in the promoters of defense-related genes and regulates pathogen-defense responses (Choi et al, 2015)

Methods

Results

Conclusion