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Decades of Genetic Research on Soybean mosaic virus Resistance in Soybean.

ABSTRACT: This review summarizes the history and current state of the known genetic basis for soybean resistance to Soybean mosaic virus (SMV), and examines how the integration of molecular markers has been utilized in breeding for crop improvement. SVM causes yield loss and seed quality reduction in soybean based on the SMV strain and the host genotype. Understanding the molecular underpinnings of SMV-soybean interactions and the genes conferring resistance to SMV has been a focus of intense research interest for decades. Soybean reactions are classified into three main responses: resistant, necrotic, or susceptible. Significant progress has been achieved that has greatly increased the understanding of soybean germplasm diversity, differential reactions to SMV strains, genotype-strain interactions, genes/alleles conferring specific reactions, and interactions among resistance genes and alleles. Many studies that aimed to uncover the physical position of resistance genes have been published in recent decades, collectively proposing different candidate genes. The studies on SMV resistance loci revealed that the resistance genes are mainly distributed on three chromosomes. Resistance has been pyramided in various combinations for durable resistance to SMV strains. The causative genes are still elusive despite early successes in identifying resistance alleles in soybean; however, a gene at the Rsv4 locus has been well validated.

SUBMITTER: Usovsky M

PROVIDER: S-EPMC9230979 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Decades of Genetic Research on <i>Soybean mosaic virus</i> Resistance in Soybean.

Usovsky Mariola M Chen Pengyin P Li Dexiao D Wang Aiming A Shi Ainong A Zheng Cuiming C Shakiba Ehsan E Lee Dongho D Canella Vieira Caio C Lee Yi Chen YC Wu Chengjun C Cervantez Innan I Dong Dekun D

Viruses 20220524 6

This review summarizes the history and current state of the known genetic basis for soybean resistance to <i>Soybean mosaic virus</i> (SMV), and examines how the integration of molecular markers has been utilized in breeding for crop improvement. SVM causes yield loss and seed quality reduction in soybean based on the SMV strain and the host genotype. Understanding the molecular underpinnings of SMV-soybean interactions and the genes conferring resistance to SMV has been a focus of intense resea ...[more]

PMID: 35746594

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Project description: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.

Project description:Resistance genes are an effective means for disease control in plants. They predominantly function by inducing a hypersensitive reaction, which results in localized cell death restricting pathogen spread. Some resistance genes elicit an atypical response, termed extreme resistance, where resistance is not associated with a hypersensitive reaction and its standard defense responses. Unlike hypersensitive reaction, the molecular regulatory mechanism(s) underlying extreme resistance is largely unexplored. One of the few known, naturally occurring, instances of extreme resistance is resistance derived from the soybean Rsv3 gene, which confers resistance against the most virulent Soybean mosaic virus strains. To discern the regulatory mechanism underlying Rsv3-mediated extreme resistance, we generated a gene regulatory network using transcriptomic data from time course comparisons of Soybean mosaic virus-G7-inoculated resistant (L29, Rsv3-genotype) and susceptible (Williams82, rsv3-genotype) soybean cultivars. Our results show Rsv3 begins mounting a defense by 6 hpi via a complex phytohormone network, where abscisic acid, cytokinin, jasmonic acid, and salicylic acid pathways are suppressed. We identified putative regulatory interactions between transcription factors and genes in phytohormone regulatory pathways, which is consistent with the demonstrated involvement of these pathways in Rsv3-mediated resistance. One such transcription factor identified as a putative transcriptional regulator was MYC2 encoded by Glyma.07G051500. Known as a master regulator of abscisic acid and jasmonic acid signaling, MYC2 specifically recognizes the G-box motif ("CACGTG"), which was significantly enriched in our data among differentially expressed genes implicated in abscisic acid- and jasmonic acid-related activities. This suggests an important role for Glyma.07G051500 in abscisic acid- and jasmonic acid-derived defense signaling in Rsv3. Resultantly, the findings from our network offer insights into genes and biological pathways underlying the molecular defense mechanism of Rsv3-mediated extreme resistance against Soybean mosaic virus. The computational pipeline used to reconstruct the gene regulatory network in this study is freely available at https://github.com/LiLabAtVT/rsv3-network.

Dataset Information

Decades of Genetic Research on Soybean mosaic virus Resistance in Soybean.

Publications

Decades of Genetic Research on <i>Soybean mosaic virus</i> Resistance in Soybean.

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