scholarly journals Precise Exchange of the Helper-Component Proteinase Cistron Between Soybean mosaic virus and Clover yellow vein virus: Impact on Virus Viability and Host Range Specificity

2020 ◽  
Vol 110 (1) ◽  
pp. 206-214 ◽  
Author(s):  
Y. Wang ◽  
W. Xu ◽  
J. Abe ◽  
K. S. Nakahara ◽  
M. R. Hajimorad
Keyword(s):  
Host Range ◽  
Mosaic Virus ◽  
Broad Bean ◽  
Soybean Mosaic Virus ◽  
Wild Soybean ◽  
Systemic Infection ◽  
Yellow Vein ◽  
Clover Yellow Vein Virus ◽  
Helper Component Proteinase ◽  
Cultivated Soybean

Soybean mosaic virus and Clover yellow vein virus are two definite species of the genus Potyvirus within the family Potyviridae. Soybean mosaic virus-N (SMV-N) is well adapted to cultivated soybean (Glycine max) genotypes and wild soybean (G. soja), whereas it remains undetectable in inoculated broad bean (Vicia faba). In contrast, clover yellow vein virus No. 30 (ClYVV-No. 30) is capable of systemic infection in broad bean and wild soybean; however, it infects cultivated soybean genotypes only locally. In this study, SMV-N was shown to also infect broad bean locally; hence, broad bean is a host for SMV-N. Based on these observations, it was hypothesized that lack of systemic infection by SMV-N in broad bean and by ClYVV-No. 30 in cultivated soybean is attributable to the incompatibility of multifunctional helper-component proteinase (HC-Pro) in these hosts. The logic of selecting the HC-Pro cistron as a target is based on its established function in systemic movement and being a relevant factor in host range specificity of potyviruses. To test this hypothesis, chimeras were constructed with precise exchanges of HC-Pro cistrons between SMV-N and ClYVV-No. 30. Upon inoculation, both chimeras were viable in infection, but host range specificity of the recombinant viruses did not differ from those of the parental viruses. These observations suggest that (i) HC-Pro cistrons from SMV-N and ClYVV-No. 30 are functionally compatible in infection despite 55.6 and 48.9% nucleotide and amino acid sequence identity, respectively, and (ii) HC-Pro cistrons from SMV-N and ClYVV-No. 30 are not the determinants of host specificity on cultivated soybean or broad beans, respectively.

scholarly journals Recessive Resistance Governed by a Major Quantitative Trait Locus Restricts Clover Yellow Vein Virus in Mechanically but Not Graft-Inoculated Cultivated Soybeans

2019 ◽  
Vol 32 (8) ◽  
pp. 1026-1037 ◽  
Author(s):  
Junya Abe ◽  
Yongzhi Wang ◽  
Tetsuya Yamada ◽  
Masako Sato ◽  
Takuya Ono ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Quantitative Trait ◽  
Major Quantitative Trait Locus ◽  
Recombinant Inbred Lines ◽  
Systemic Infection ◽  
Yellow Vein ◽  
Systemic Spread ◽  
Clover Yellow Vein Virus ◽  
Trait Locus ◽  
Cultivated Soybean

Clover yellow vein virus (ClYVV) infects and causes disease in legume plants. However, here, we found that ClYVV isolate No. 30 (ClYVV-No.30) inefficiently multiplied or spread via cell-to-cell movement in mechanically inoculated leaves of a dozen soybean (Glycine max) cultivars and resulted in failure to spread systemically. Soybean plants also had a similar resistance phenotype against additional ClYVV isolates. In contrast, all but one of 24 tested accessions of wild soybeans (G. soja) were susceptible to ClYVV-No.30. Graft inoculation of cultivated soybean TK780 with ClYVV-No.30–infected wild soybean B01167 scion resulted in systemic infection of the cultivated soybean rootstock. This suggests that, upon mechanical inoculation, the cultivated soybean inhibits ClYVV-No.30, at infection steps prior to the systemic spread of the virus, via vascular systems. Systemic infection of all F1 plants from crossing between TK780 and B01167 and of 68 of 76 F2 plants with ClYVV-No.30 indicated recessive inheritance of the resistance. Further genetic analysis using 64 recombinant inbred lines between TK780 and B01167 detected one major quantitative trait locus, designated d-cv, for the resistance that was positioned in the linkage group D1b (chromosome 2). The mapped region on soybean genome suggests that d-cv is not an allele of the known resistance genes against soybean mosaic virus.

Multiple genes confer resistance to soybean mosaic virus in the soybean cultivar Hwangkeum

2014 ◽  
Vol 12 (S1) ◽  
pp. S41-S44 ◽  
Author(s):  
Namhee Jeong ◽  
Soon-Chun Jeong
Keyword(s):  
Mosaic Virus ◽  
Recombinant Inbred Lines ◽  
Soybean Mosaic Virus ◽  
Durable Resistance ◽  
Wild Soybean ◽  
Soybean Cultivar ◽  
Breeding Programmes ◽  
Cultivated Species ◽  
Cultivated Soybean ◽  
Efficient Selection

Recombinant inbred lines (RILs) generated from a cross between a cultivated species and its wild progenitor species serve as important germplasm for introgressing valuable genes from a wild species to a cultivated species. During this breeding process, it is equally important to prevent the loss of agronomically important genes in the cultivated species. In an effort to establish an efficient selection system for the single Rsv1 gene conferring durable resistance to soybean mosaic virus (SMV) in the soybean cultivar Hwangkeum (also known as Suweon 97), which is a parent of a RIL population from Hwangkeum (cultivated soybean) × IT182932 (wild soybean), in the present study, we unexpectedly identified an additional necrosis-conditioning gene unmasked by a recombination in the middle of the Rsv1-containing nucleotide-binding leucine-rich repeat gene cluster region and the Rsv3 gene in Hwangkeum. Thus, Hwangkeum contains at least three SMV resistance genes consisting of two tightly linked genes at the Rsv1 locus and the Rsv3 locus. The results of this study provide additional important information for use of the Hwangkeum genome in soybean breeding programmes.

scholarly journals Adaptation of Soybean mosaic virus Avirulent Chimeras Containing P3 Sequences from Virulent Strains to Rsv1-Genotype Soybeans Is Mediated by Mutations in HC-Pro

2008 ◽  
Vol 21 (7) ◽  
pp. 937-946 ◽  
Author(s):  
M. R. Hajimorad ◽  
A. L. Eggenberger ◽  
J. H. Hill
Keyword(s):  
Amino Acids ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Soybean Mosaic Virus ◽  
Extreme Resistance ◽  
Sequence Analyses ◽  
Virulent Strains ◽  
N Terminus ◽  
Helper Component Proteinase ◽  
Avirulent Isolate

In Rsv1-genotype soybean, Soybean mosaic virus (SMV)-N (an avirulent isolate of strain G2) elicits extreme resistance (ER) whereas strain SMV-G7 provokes a lethal systemic hypersensitive response (LSHR). SMV-G7d, an experimentally evolved variant of SMV-G7, induces systemic mosaic. Thus, for Rsv1-genotype soybean, SMV-N is avirulent whereas SMV-G7 and SMV-G7d are both virulent. Exploiting these differential interactions, we recently mapped the elicitor functions of SMV provoking Rsv1-mediated ER and LSHR to the N-terminal 271 amino acids of P3 from SMV-N and SMV-G7, respectively. The phenotype of both SMV-G7 and SMV-G7d were rendered avirulent on Rsv1-genotype soybean when the part of the genome encoding the N-terminus or the entire P3 cistron was replaced with that from SMV-N; however, reciprocal exchanges did not confer virulence to SMV-N-derived P3 chimeras. Here, we describe virulent SMV-N-derived P3 chimeras containing the full-length or the N-terminal P3 from SMV-G7 or SMV-G7d, with or without additional mutations in P3, that were selected on Rsv1-genotype soybean by sequential transfers on rsv1 and Rsv1-genotype soybean. Sequence analyses of the P3 and helper-component proteinase (HC-Pro) cistrons of progeny recovered from Rsv1-genotype soybean consistently revealed the presence of mutations in HC-Pro. Interestingly, the precise mutations in HC-Pro required for the adaptation varied among the chimeras. No mutation was detected in the HC-Pro of progeny passaged continuously in rsv1-genotype soybean, suggesting that selection is a consequence of pressure imposed by Rsv1. Mutations in HC-Pro alone failed to confer virulence to SMV-N; however, reconstruction of mutations in HC-Pro of the SMV-N-derived P3 chimeras resulted in virulence. Taken together, the data suggest that HC-Pro complementation of P3 is essential for SMV virulence on Rsv1-genotype soybean.

scholarly journals P3N-PIPO, a Frameshift Product from theP3Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

2016 ◽  
Vol 90 (16) ◽  
pp. 7388-7404 ◽  
Author(s):  
Go Atsumi ◽  
Haruka Suzuki ◽  
Yuri Miyashita ◽  
Sun Hee Choi ◽  
Yusuke Hisa ◽  
...  
Keyword(s):  
Cell Death ◽  
Resistance Gene ◽  
Systemic Infection ◽  
Viral Disease ◽  
Hypersensitive Reaction ◽  
Yellow Vein ◽  
Recessive Resistance ◽  
Content Type ◽  
Clover Yellow Vein Virus ◽  
And Control

ABSTRACTPeas carrying thecyv1recessive resistance gene are resistant to clover yellow vein virus (ClYVV) isolates No.30 (Cl-No.30) and 90-1 (Cl-90-1) but can be infected by a derivative of Cl-90-1 (Cl-90-1 Br2). The main determinant for the breaking ofcyv1resistance by Cl-90-1 Br2 is P3N-PIPO produced from theP3gene via transcriptional slippage, and the higher level of P3N-PIPO produced by Cl-90-1 Br2 than by Cl-No.30 contributes to the breaking of resistance. Here we show that P3N-PIPO is also a major virulence determinant in susceptible peas that possess another resistance gene,Cyn1, which does not inhibit systemic infection with ClYVV but causes hypersensitive reaction-like lethal systemic cell death. We previously assumed that the susceptible pea cultivar PI 226564 has a weak allele ofCyn1. Cl-No.30 did not induce cell death, but Cl-90-1 Br2 killed the plants. Our results suggest that P3N-PIPO is recognized byCyn1and induces cell death. Unexpectedly, heterologously strongly expressed P3N-PIPO of Cl-No.30 appears to be recognized byCyn1in PI 226564. The level of P3N-PIPO accumulation from theP3gene of Cl-No.30 was significantly lower than that of Cl-90-1 Br2 in aNicotiana benthamianatransient assay. Therefore,Cyn1-mediated cell death also appears to be determined by the level of P3N-PIPO. The more efficiently a ClYVV isolate brokecyv1resistance, the more it induced cell death systemically (resulting in a loss of the environment for virus accumulation) in susceptible peas carryingCyn1, suggesting that antagonistic pleiotropy of P3N-PIPO controls the resistance breaking of ClYVV.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 bycyv1, 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 acyv1-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 dominantCyn1gene, which may impose evolutionary constraints uponP3N-PIPOfor overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.

scholarly journals Gain of Virulence on Rsv1-Genotype Soybean by an Avirulent Soybean mosaic virus Requires Concurrent Mutations in Both P3 and HC-Pro

2008 ◽  
Vol 21 (7) ◽  
pp. 931-936 ◽  
Author(s):  
A. L. Eggenberger ◽  
M. R. Hajimorad ◽  
J. H. Hill
Keyword(s):  
Amino Acids ◽  
Mosaic Virus ◽  
Resistance Gene ◽  
Hypersensitive Response ◽  
Soybean Mosaic Virus ◽  
Cytoplasmic Inclusion ◽  
Virulence Determinants ◽  
Extreme Resistance ◽  
Helper Component ◽  
Helper Component Proteinase

In soybean, Rsv1, a single dominant resistance gene, invokes extreme resistance (ER) against most Soybean mosaic virus (SMV) strains, including SMV-N, but not SMV-G7, which provokes a virulent lethal systemic hypersensitive response (LSHR). The elicitor functions of the two viruses provoking Rsv1-mediated ER and LSHR have been mapped to the N-terminal 271 amino acids of P3 from SMV-N and SMV-G7, respectively, which differ by nine residues between the two strains. To identify amino acids of P3 from SMV-N provoking Rsv1-mediated ER, the unique residues of SMV-G7 were substituted with those of SMV-N. Of the mutants tested on Rsv1-genotype soybean, only SMV-G7I788R and SMV-G7T948A lost virulence. However, substitution of amino acids of SMV-N, individually or in combination, with the reciprocal residues from SMV-G7 at these two positions failed to confer virulence to SMV-N. In the search for additional virulence determinants, a series of SMV-N chimeras was generated in which fragments within a region from near the middle of the helper-component proteinase (HC-Pro) cistron to the 5′ end of the cytoplasmic inclusion cistron, nucleotides 1,605 to 3,787, were replaced with those of SMV-G7. Only SMV-N-derived chimeras harboring the 3′ region of HC-Pro, at least from nucleotide 2,013, and the entire 5′ end of P3 (nucleotides 2,430 to 3,237) from SMV-G7 were virulent whereas reciprocal exchanges resulted in loss of SMV-G7 virulence. This region of HC-Pro differs by three amino acids between SMV-N and SMV-G7. Analyses of SMV-G7-derived HC-Pro site-directed mutants showed that only SMV-G7M683R lost virulence on Rsv1-genotype soybean; however, SMV-NR682M failed to gain virulence. Nevertheless, an SMV-N derived mutant with three concurrent substitutions, R682M+R787I+A947T, gained virulence. The data indicate that both P3 and HC-Pro are involved in virulence of SMV on Rsv1-genotype soybean.

White clover (Trifolium repens) and associated viruses in the subalpine region of south-eastern Australia: implications for GMO risk assessment

2004 ◽  
Vol 52 (3) ◽  
pp. 321 ◽  
Author(s):  
R. C. Godfree ◽  
P. W. G. Chu ◽  
M. J. Woods
Keyword(s):  
Mosaic Virus ◽  
Plant Communities ◽  
White Clover ◽  
Alfalfa Mosaic Virus ◽  
Yellow Vein ◽  
Native Plant ◽  
Eastern Australia ◽  
Clover Yellow Vein Virus ◽  
Subalpine Region ◽  
White Clover Mosaic Virus

Over the past several years, increased emphasis has been placed on conducting comprehensive ecological-risk assessments of virus-resistant genetically modified organisms (GMOs) prior to their release into the environment. In this paper we report on the first stage in our assessment of the level of risk posed by virus-resistant transgenic Trifolium repens L. (white clover) to native plant communities in south-eastern Australia. We investigated the distribution, abundance and phytosociological characteristics of naturalised T. repens populations in two areas in the subalpine region of New South Wales (NSW) and the Australian Capital Territory (ACT), and determined the distribution and abundance of Alfalfa mosaic virus, Clover yellow vein virus and White clover mosaic virus in 31 populations of white clover in this region. We found that T. repens is a significant component of Poa grasslands and Eucalyptus–Poa woodlands in the subalpine region, but is absent or rare in Eucalyptus species forests and Carex–Poa species bogs. Clover yellow vein virus was by far the most common virus in the study area, being present in 18% of T. repens plants across a wide range of plant communities. Alfalfa mosaic virus and White clover mosaic virus were each recorded in only one white-clover population growing in a native plant community. We conclude that white clover is a significant constituent of subalpine grasslands and woodlands in the region studied, and that of the viruses investigated, Clover yellow vein virus is the most abundant and widespread.

Screening for pathotype-specific resistance to broad bean wilt virus 2 and cucumber mosaic virus in pepper (Capsicum annuum L.)

2021 ◽  
pp. 1-6
Author(s):  
Kyeong-Jae Heo ◽  
Boram Choi ◽  
Myung-Hwi Kim ◽  
Min-Jun Kwon ◽  
Young-Eun Cho ◽  
...  
Keyword(s):  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Broad Bean ◽  
Specific Resistance ◽  
Systemic Infection ◽  
Cdna Clones ◽  
Breeding Programs ◽  
Population Structures ◽  
Wilt Virus ◽  
Broad Bean Wilt Virus

Abstract Two aphid-transmitted RNA viruses, broad bean wilt virus 2 (BBWV2) and cucumber mosaic virus (CMV), are the most prevalent viruses in Korean pepper fields and cause chronic damage in pepper production. In this study, we employed a screening system for pathotype-specific resistance of pepper germplasm to BBWV2 and CMV by utilizing infectious cDNA clones of different pathotypes of the viruses (two BBWV2 strains and three CMV strains). We first examined pathogenic characteristics of the BBWV2 and CMV strains in various plant species and their phylogenetic positions in the virus population structures. We then screened 34 commercial pepper cultivars and seven accessions for resistance. While 21 pepper cultivars were resistant to CMV Fny strain, only two cultivars were resistant to CMV P1 strain. We also found only one cultivar partially resistant to BBWV2 RP1 strain. However, all tested commercial pepper cultivars were susceptible to the resistance-breaking CMV strain GTN (CMV-GTN) and BBWV2 severe strain PAP1 (BBWV2-PAP1), suggesting that breeding new cultivars resistant to these virus strains is necessary. Fortunately, we identified several pepper accessions that were resistant or partially resistant to CMV-GTN and one symptomless accession despite systemic infection with BBWV2-PAP1. These genetic resources will be useful in pepper breeding programs to deploy resistance to BBWV2 and CMV.

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