Overexpression of GmAKT2 potassium channel enhances resistance to soybean mosaic virus.

Lian Zhou,Huixia Shou,Hongli He,Qiang Han,Bao Liu,Ruifang Liu

doi:10.1186/1471-2229-14-154

Abstract

BackgroundSoybean mosaic virus (SMV) is the most prevalent viral disease in many soybean production areas. Due to a large number of SMV resistant loci and alleles, SMV strains and the rapid evolution in avirulence/effector genes, traditional breeding for SMV resistance is complex. Genetic engineering is an effective alternative method for improving SMV resistance in soybean. Potassium (K+) is the most abundant inorganic solute in plant cells, and is involved in plant responses to abiotic and biotic stresses. Studies have shown that altering the level of K+ status can reduce the spread of the viral diseases. Thus K+ transporters are putative candidates to target for soybean virus resistance.ResultsThe addition of K+ fertilizer significantly reduced SMV incidence. Analysis of K+ channel gene expression indicated that GmAKT2, the ortholog of Arabidopsis K+ weak channel encoding gene AKT2, was significantly induced by SMV inoculation in the SMV highly-resistant genotype Rsmv1, but not in the susceptible genotype Ssmv1. Transgenic soybean plants overexpressing GmAKT2 were produced and verified by Southern blot and RT-PCR analysis. Analysis of K+ concentrations on different leaves of both the transgenic and the wildtype (Williams 82) plants revealed that overexpression of GmAKT2 significantly increased K+ concentrations in young leaves of plants. In contrast, K+ concentrations in the old leaves of the GmAKT2-Oe plants were significantly lower than those in WT plants. These results indicated that GmAKT2 acted as a K+ transporter and affected the distribution of K+ in soybean plants. Starting from 14 days after inoculation (DAI) of SMV G7, severe mosaic symptoms were observed on the WT leaves. In contrast, the GmAKT2-Oe plants showed no symptom of SMV infection. At 14 and 28 DAI, the amount of SMV RNA in WT plants increased 200- and 260- fold relative to GmAKT2-Oe plants at each time point. Thus, SMV development was significantly retarded in GmAKT2-overexpressing transgenic soybean plants.ConclusionsOverexpression of GmAKT2 significantly enhanced SMV resistance in transgenic soybean. Thus, alteration of K+ transporter expression is a novel molecular approach for enhancing SMV resistance in soybean.

Highlights

Soybean mosaic virus (SMV) is the most prevalent viral disease in many soybean production areas
The effect of K+ supply on SMV incidence To investigate whether K+ supply affected the resistance of soybean plants to SMV, the susceptible soybean cultivar Williams 82 was planted in pots containing low-K+ soil with or without the addition of K+ fertilizer
K+ concentrations in the old leaves of the GmAKT2-Oe plants were significantly lower than those in the WT plants (Figure 5A, 5B). These results indicated that GmAKT2 acted as a K+ transporter and affected the distribution of K+ in soybean plants

Summary

Introduction

K+ transporters are putative candidates to target for soybean virus resistance. Soybean mosaic virus (SMV) is the most prevalent viral disease in many soybean production areas [1]. There are seven SMV strain groups (G1-G7) and three resistance loci (Rsv, Rsv, and Rsv4) reported in soybean [5,6,7,8]. Soybean germplasm with Rsv locus are resistant to SMV strain groups G1-G3, but susceptible to strains G5G7 [9]. Lines containing Rsv confer resistance to strain groups G5-G7, and condition stem-tip necrosis and/or mosaic symptoms to G1-G4 [10]. The Rsv locus was reported to produce seedling resistance to most SMV isolates but systemic symptoms can appear as plants mature [11]. Rsv was shown to link to a cluster of six non-Toll interleukin

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Discussion

Conclusion