Fitness penalty in susceptible host is associated with virulence of <i><scp>S</scp>oybean mosaic virus</i> on <i><scp>R</scp>sv1</i>‐genotype soybean: a consequence of perturbation of <scp>HC</scp>‐<scp>P</scp>ro and not <scp>P</scp>3

Khatabi, Behnam; Wen, R.-H.; Hajimorad, M. R.

doi:10.1111/mpp.12054

Cited by 25 publications

(29 citation statements)

References 99 publications

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“…One such approach is through evaluation of fitness effects of individual genes (Fabre et al, 2009; Janzac et al, 2009; Khatabi et al, 2013; Leach et al, 2001; Vera Cruz 2000). If avirulence genes also function as virulence effectors (Cunnac et al, 2001; Jones and Dangl, 2006), then durability might reasonably be expected to be correlated with the fitness reduction associated with loss of the effector, and combining genes with large fitness losses would be expected to be more durable than combining genes with little or no fitness reduction.…”

Section: Deployment Strategiesmentioning

confidence: 99%

Durable resistance: A key to sustainable management of pathogens and pests

Mundt

2014

Infection, Genetics and Evolution

308

255

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This review briefly addresses what has been learned about resistance durability in recent years, as well as the questions that still remain. Molecular analyses of major gene interactions have potential to contribute to both breeding for resistance and improved understanding of virulence impacts on pathogen fitness. Though the molecular basis of quantitative resistance is less clear substantial evidence has accumulated for the relative simplicity of inheritance. There is increasing evidence for specific interactions with quantitative resistance, though implications o this for durability are still unknown. Mechanisms by which resistance gene pyramids contribute to durability remain elusive, though ideas have been generated for identifying gene combinations that may be more durable. Though cultivar mixtures and related approaches have been used successfully, identifying the diseases and conditions that are most conducive to the use of diversity has been surprisingly difficult, and the selective influence of diversity on pathogen populations is complex. The importance of considering resistance durability in a landscape context has received increasing emphasis and is an important future area of research. Experimental systems are being developed to test resistance gene deployment strategies that previously could be addressed only with logic and observation. The value of molecular markers for identifying and pyramiding major genes is quite clear, but the successful use of quantitative trait loci (QTL) for marker-assisted selection of quantitative resistance will depend greatly on the degree to which the identified QTL are expressed in different genetic backgrounds. Transgenic approaches will likely provide opportunities for control of some recalcitrant pathogens, though issues of durability for transgenes are likely to be no different than other genes for resistance. The need for high quality phenotypic analysis and screening methodologies is a priority, and field-based studies are likely to remain of signal importance in the foreseeable future.

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Section: Deployment Strategiesmentioning

confidence: 99%

Durable resistance: A key to sustainable management of pathogens and pests

Mundt

2014

Infection, Genetics and Evolution

308

255

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“…In contrast, the line L943 lacks 3gG2, but contains a suite of five other NBS-LRR genes allows limited replication of SMV-N at the inoculation site. Domain swapping experiments between SMV-N and SMV-G7/SMV-G7d demonstrate that at least two distinct resistance genes at the Rsv1 locus, probably belonging to the NBS-LRR class, mediate recognition of HC-Pro and P3, respectively (Khatabi et al, 2013; Yang et al, 2013). …”

Section: Mapping Of Smv Resistant Locimentioning

confidence: 99%

“…It seems that it is a common phenomenon that gain of virulence mutation(s) by an avirulent SMV strain on a resistant genotype soybean is associated with a relative fitness loss (reduced pathogenicity or virulence) in a susceptible host (Khatabi et al, 2013; Wang and Hajimorad, 2016). The majority of experimentally evolved mutations that disrupt the avirulence functions of SMV-N on Rsv1 -genotype soybean also results in mild symptoms and reduced virus accumulation, relative to parental SMV-N, in Williams82 ( rsv1 ), demonstrating that gain of virulence by SMV on Rsv1 -genotype soybean results in fitness loss in a previously susceptible soybean genotype, which is resulted from mutations in HC-Pro, and not in P3 (Khatabi et al, 2013; Wang and Hajimorad, 2016).…”

Section: Gain Of Virulence By Smv On a Resistant Soybean Genotype Resmentioning

confidence: 99%

“…The majority of experimentally evolved mutations that disrupt the avirulence functions of SMV-N on Rsv1 -genotype soybean also results in mild symptoms and reduced virus accumulation, relative to parental SMV-N, in Williams82 ( rsv1 ), demonstrating that gain of virulence by SMV on Rsv1 -genotype soybean results in fitness loss in a previously susceptible soybean genotype, which is resulted from mutations in HC-Pro, and not in P3 (Khatabi et al, 2013; Wang and Hajimorad, 2016). It has been also demonstrated that gain of virulence mutation(s) by all avirulent viruses on Rsv4 -genotype soybean is associated with a relative fitness penalty for gaining virulence by an avirulence strain (Wang and Hajimorad, 2016).…”

Section: Gain Of Virulence By Smv On a Resistant Soybean Genotype Resmentioning

confidence: 99%

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The Current Status of the Soybean-Soybean Mosaic Virus (SMV) Pathosystem

2016

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Soybean mosaic virus (SMV) is one of the most devastating pathogens that cost huge economic losses in soybean production worldwide. Due to the duplicated genome, clustered and highly homologous nature of R genes, as well as recalcitrant to transformation, soybean disease resistance studies is largely lagging compared with other diploid crops. In this review, we focus on the major advances that have been made in identifying both the virulence/avirulence factors of SMV and mapping of SMV resistant genes in soybean. In addition, we review the progress in dissecting the SMV resistant signaling pathways in soybean, with a special focus on the studies using virus-induced gene silencing. The soybean genome has been fully sequenced, and the increasingly saturated SNP markers have been identified. With these resources available together with the newly developed genome editing tools, and more efficient soybean transformation system, cloning SMV resistant genes, and ultimately generating cultivars with a broader spectrum resistance to SMV are becoming more realistic than ever.

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“…Soybeans carrying the dominant Rsv1 or Rsv4 allele are resistant to SMV-N (62) or three strains (SMV-N, SMV-G7, and SMV-G7d) (63), respectively. SMV-N HC-Pro mutants or SMV P3 mutants of the three strains can overcome these respective resistances, and the accumulation of these mutants is reduced in susceptible cultivars (62,63). Those studies indicated that their fitness tradeoffs are caused by antagonistic pleiotropy of the viral genes that overcome dominant resistance.…”

Section: Discussionmentioning

confidence: 93%

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

Atsumi

Suzuki

Miyashita

et al. 2016

J Virol

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IMPORTANCEControl of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred by cyv1, mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in a cyv1-carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance (cyv1) and host viability; the latter is presumably regulated by the dominant Cyn1 gene, which may impose evolutionary constraints upon P3N-PIPO for overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.H ost plants protect themselves from virus infection by activating defense systems mediated by immune receptors (e.g., nucleotide-binding-site-leucine-rich-repeat [NB-LRR] proteins) (1). Plants have many NB-LRR immune receptors, each of which recognizes specific viral proteins. The activated immune response is referred to as a hypersensitive response (HR) and is often accompanied by cell death. When an HR is induced, the virus is localized in and around the infection locus. NB-LRR immune receptors are encoded by resistance genes that are genetically dominant.Another important defense against plant virus infection is genetically recessive resistance (2). The viral life cycle totally relies on host cells, and viruses require host factors in order to multiply within cells and move to neighboring cells. Therefore, the lack of a specific host-coopted factor required for the viral life cycle leads to host resistance against the virus, which would be recessively inherited. Many natural recessive resistance genes against viruses have been identified in diverse crops (2). Extensive studies have been carried out on viruses belonging to the Potyvirus genus, the major genus of the Potyviridae family, which is one of the two largest plant virus genera and is found in most climatic regions worldwide (3). These viruses infect a broad range of host plants, including both monocots and dicots. They cause considerable crop damage, resulting in severe economic losses. Most of the recessive

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Fitness penalty in susceptible host is associated with virulence of Soybean mosaic virus on Rsv1‐genotype soybean: a consequence of perturbation of HC‐Pro and not P3

Cited by 25 publications

References 99 publications

Durable resistance: A key to sustainable management of pathogens and pests

Durable resistance: A key to sustainable management of pathogens and pests

The Current Status of the Soybean-Soybean Mosaic Virus (SMV) Pathosystem

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

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