scholarly journals The HC-Pro and P3 Cistrons of an Avirulent Soybean mosaic virus Are Recognized by Different Resistance Genes at the Complex Rsv1 Locus

2013 ◽  
Vol 26 (2) ◽  
pp. 203-215 ◽  
Author(s):  
R.-H. Wen ◽  
B. Khatabi ◽  
T. Ashfield ◽  
M. A. Saghai Maroof ◽  
M. R. Hajimorad
Keyword(s):  
Mosaic Virus ◽  
Resistance Genes ◽  
Soybean Mosaic Virus ◽  
Plant Introduction ◽  
Soybean Plant ◽  
Leucine Rich Repeat ◽  
Extreme Resistance ◽  
Helper Component ◽  
Inoculation Site ◽  
Helper Component Proteinase

The complex Rsv1 locus in soybean plant introduction (PI) ‘PI96983’ confers extreme resistance (ER) against Soybean mosaic virus (SMV) strain N but not SMV-G7 and SMV-G7d. Both the SMV helper-component proteinase (HC-Pro) and P3 cistrons can serve as avirulence factors recognized by Rsv1. To understand the genetics underlying recognition of the two cistrons, we have utilized two soybean lines (L800 and L943) derived from crosses between PI96983 (Rsv1) and Lee68 (rsv1) with distinct recombination events within the Rsv1 locus. L800 contains a single PI96983-derived member (3gG2) of an Rsv1-associated subfamily of nucleotide-binding leucine-rich repeat (NB-LRR) genes. In contrast, although L943 lacks 3gG2, it contains a suite of five other NB-LRR genes belonging to the same family. L800 confers ER against SMV-N whereas L943 allows limited replication at the inoculation site. SMV-N-derived chimeras containing HC-Pro from SMV-G7 or SMV-G7d gained virulence on L943 but not on L800 whereas those with P3 replacement gained virulence on L800 but not on L943. In reciprocal experiments, SMV-G7- and SMV-G7d-derived chimeras with HC-Pro replacement from SMV-N lost virulence on L943 but retained virulence on L800 whereas those with P3 replacement lost virulence on L800 while remaining virulent on L943. These data demonstrate that distinct resistance genes at the Rsv1 locus, likely belonging to the NB-LRR class, mediate recognition of HC-Pro and P3.

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.

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 The Requirement of Multiple Defense Genes in Soybean Rsv1–Mediated Extreme Resistance to Soybean mosaic virus

2012 ◽  
Vol 25 (10) ◽  
pp. 1307-1313 ◽  
Author(s):  
Chunquan Zhang ◽  
Sehiza Grosic ◽  
Steven A. Whitham ◽  
John H. Hill
Keyword(s):  
Transcription Factors ◽  
Mosaic Virus ◽  
Resistance Genes ◽  
Target Genes ◽  
Soybean Mosaic Virus ◽  
Virus Induced Gene Silencing ◽  
Wrky Transcription Factors ◽  
Extreme Resistance ◽  
Viral Pathogen ◽  
Insight Into

Soybean mosaic virus (SMV) is a major viral pathogen of soybean. Among the three SMV resistance genes, Rsv1 mediates extreme resistance (ER) against most SMV strains, including the β-glucuronidase-tagged G2 isolate that was previously used in studies of Rsv1. Using virus-induced gene silencing (VIGS), we screened 82 VIGS constructs to identify genes that play a role in Rsv1-mediated ER to SMV infection. The target genes included putative Rsv1 candidate genes, soybean orthologs to known defense-signaling genes, and 62 WRKY transcription factors. We identified eight VIGS constructs that compromised Rsv1-mediated resistance when the target genes were silenced, including GmEDR1, GmEDS1, GmHSP90, GmJAR1, GmPAD4, and two WRKY transcription factors. Together, our results provide new insight into the soybean signaling network required for ER against SMV.

scholarly journals Role of Soybean mosaic virus–Encoded Proteins in Seed and Aphid Transmission in Soybean

2013 ◽  
Vol 103 (9) ◽  
pp. 941-948 ◽  
Author(s):  
Sushma Jossey ◽  
Houston A. Hobbs ◽  
Leslie L. Domier
Keyword(s):  
Mosaic Virus ◽  
Seed Quality ◽  
Soybean Mosaic Virus ◽  
Seed Transmission ◽  
Aphid Transmission ◽  
Plant Introduction ◽  
Sequence Motif ◽  
Coding Region ◽  
Encoded Proteins ◽  
Seed Transmissibility

Soybean mosaic virus (SMV) is seed and aphid transmitted and can cause significant reductions in yield and seed quality in soybean (Glycine max). The roles in seed and aphid transmission of selected SMV-encoded proteins were investigated by constructing mutants in and chimeric recombinants between SMV 413 (efficiently aphid and seed transmitted) and an isolate of SMV G2 (not aphid or seed transmitted). As previously reported, the DAG amino acid sequence motif near the amino terminus of the coat protein (CP) was the major determinant in differences in aphid transmissibility of the two SMV isolates, and helper component proteinase (HC-Pro) played a secondary role. Seed transmission of SMV was influenced by P1, HC-Pro, and CP. Replacement of the P1 coding region of SMV 413 with that of SMV G2 significantly enhanced seed transmissibility of SMV 413. Substitution in SMV 413 of the two amino acids that varied in the CPs of the two isolates with those from SMV G2, G to D in the DAG motif and Q to P near the carboxyl terminus, significantly reduced seed transmission. The Q-to-P substitution in SMV 413 also abolished virus-induced seed-coat mottling in plant introduction 68671. This is the first report associating P1, CP, and the DAG motif with seed transmission of a potyvirus and suggests that HC-Pro interactions with CP are important for multiple functions in the virus infection cycle.

scholarly journals Similarities in Seed and Aphid Transmission Among Soybean mosaic virus Isolates

Plant Disease ◽  
2007 ◽  
Vol 91 (5) ◽  
pp. 546-550 ◽  
Author(s):  
Leslie L. Domier ◽  
Todd A. Steinlage ◽  
Houston A. Hobbs ◽  
Yi Wang ◽  
Gabriel Herrera-Rodriguez ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Field Experiments ◽  
Soybean Mosaic Virus ◽  
Aphid Transmission ◽  
Amino Acid Sequences ◽  
Mechanical Transmission ◽  
Soybean Plant ◽  
Loss Of Function ◽  
Strain Specificity ◽  
Plant Introductions

Soybean mosaic virus (SMV) is an aphid- and seed-transmitted virus that infects soybean (Glycine max) plants and causes significant yield losses. Seed-borne infections are the primary sources of inoculum for SMV infections. The strain specificity of SMV transmission through seed and SMV-induced seed-coat mottling were investigated in field experiments. Six soybean plant introductions (PIs) were inoculated with eight SMV strains and isolates. Transmission of SMV through seed ranged from 0 to 43%, and isolate-by-soybean line interactions occurred in both transmission rates and percentages of mottled seeds. For example, SMV 746 was transmitted through 43% of seed in PI 229324, but was not transmitted through seed of PIs 68522, 68671, or 86449. In contrast, SMV 413 was transmitted through seed from all PIs. SMVs that were transmitted poorly by the Asian soybean aphid, Aphis glycines, also were transmitted poorly through seed. No predicted amino acid sequences within the helper-component protease or coat protein coding regions differentiated the two groups of SMV strains. The loss of aphid and seed transmissibility by repeated mechanical transmission suggests that constant selection pressure is needed to maintain the regions of the SMV genome controlling the two phenotypes from genetic drift and loss of function.

Genetic analysis and fine-mapping of Soybean mosaic virus SC7 and SC13 resistance genes in soybean (Glycine max)

2020 ◽  
Vol 71 (5) ◽  
pp. 477
Author(s):  
Hexiang Luan ◽  
Yongkun Zhong ◽  
Dagang Wang ◽  
Rui Ren ◽  
Le Gao ◽  
...  
Keyword(s):  
Glycine Max ◽  
Mosaic Virus ◽  
Resistance Genes ◽  
Fine Mapping ◽  
Soybean Mosaic Virus ◽  
Resistance Breeding ◽  
Physical Distance ◽  
Breeding Systems ◽  
Chromosome 2 ◽  
Transcription Factor Genes

Soybean mosaic virus (SMV) is one of the most destructive pathogens of soybean (Glycine max (L.) Merr.) worldwide. In this study, 184 F7:11 recombinant inbred line (RIL) populations derived from Kefeng No. 1 × Nannong 1138-2 were used to study the inheritance and linkage mapping of resistance genes against SMV strains SC7 and SC13 in Kefeng No. 1. Two independent dominant genes (designated Rsc7 and Rsc13) that control resistance to SC7 and SC13 were located on a molecular linkage group (MLG) of chromosome 2 (D1b). A mixed segregating population was developed by self-pollination of three heterozygous plants of residual heterozygous lines (RHL3-27, RHL3-30, RHL3-53) with five markers linked to the loci, and was used in fine-mapping of Rsc7 and Rsc13. In addition, Rsc7 was fine-mapped between BARCSOYSSR_02_0667 and BARCSOYSSR_02_0670 on MLG D1b. The genetic distance between the two closest markers was 0.7 cM and the physical distance of the interval was ~77 kb, which included one LRR gene and another gene containing an F-box region. Two SSR markers (BARCSOYSSR_02_0610 and BARCSOYSSR_02_0621) were closely linked to the SC13 resistance gene. The physical distance where Rsc13 was located was ~191 kb. Sequence analysis showed that there were two K-box region types of transcription factor genes; GmHSP40 and two serine/threonine protein kinase (STK) genes were the most likely candidate genes. These results will facilitate map-based cloning of the Rsc7 and Rsc13 genes and development of transgenic disease-resistant varieties, and will provide SMV-resistance breeding systems with excellent resistance germplasm.

Inheritance and Allelic Relationships of Resistance Genes for Soybean mosaic virus in ‘Corsica’ and ‘Beeson’ Soybean

Crop Science ◽  
2013 ◽  
Vol 53 (4) ◽  
pp. 1455-1463 ◽  
Author(s):  
Ehsan Shakiba ◽  
Pengyin Chen ◽  
Ainong Shi ◽  
Dexiao Li ◽  
Dekun Dong ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Resistance Genes ◽  
Soybean Mosaic Virus

Soybean mosaic virus helper component-protease enhances somatic embryo production and stabilizes transgene expression in soybean

2005 ◽  
Vol 43 (10-11) ◽  
pp. 1014-1021 ◽  
Author(s):  
Hyoun-Sub Lim ◽  
Tae-Seok Ko ◽  
Kris N. Lambert ◽  
Hong-Gi Kim ◽  
Schuyler S. Korban ◽  
...  
Keyword(s):  
Somatic Embryo ◽  
Mosaic Virus ◽  
Transgene Expression ◽  
Soybean Mosaic Virus ◽  
Embryo Production ◽  
Helper Component ◽  
Somatic Embryo Production

scholarly journals Strain-Specific Cylindrical Inclusion Protein of Soybean mosaic virus Elicits Extreme Resistance and a Lethal Systemic Hypersensitive Response in Two Resistant Soybean Cultivars

2009 ◽  
Vol 22 (9) ◽  
pp. 1151-1159 ◽  
Author(s):  
Jang-Kyun Seo ◽  
Suk-Ha Lee ◽  
Kook-Hyung Kim
Keyword(s):  
Amino Acid ◽  
Mosaic Virus ◽  
Amino Acid Substitution ◽  
Hypersensitive Response ◽  
Soybean Mosaic Virus ◽  
Cylindrical Inclusion ◽  
Single Amino Acid ◽  
Extreme Resistance ◽  
Soybean Genotypes ◽  
Pathogenic Determinant

In the Soybean mosaic virus (SMV)–soybean pathosystem, three independent genes (Rsv1, Rsv3, and Rsv4) conferring resistance to SMV have been identified. Recently, we constructed infectious cDNA clones of SMV G7H and G5H strains and found that these two strains differ in their ability to infect soybean genotypes possessing different SMV resistance genes despite a difference of only 33 amino acids. In particular, pSMV-G7H induced mosaic symptoms systemically in L29 (Rsv3) and provoked a lethal systemic hypersensitive response (LSHR) in Jinpumkong-2, whereas pSMV-G5H could not infect these soybean genotypes. To identify the responsible pathogenic determinants of SMV, we exploited the differential responses of pSMV-G7H- and pSMV-G5H-derived chimeric viruses and amino acid substitution mutant viruses in several soybean genotypes and demonstrated that cylindrical inclusion (CI) protein is the elicitor of Rsv3-mediated extreme resistance and a pathogenic determinant provoking LSHR in Jinpumkong-2. A single amino acid substitution in CI was found to be responsible for gain or loss of elicitor function of CI. Our finding provides a role for CI as a pathogenic determinant in the SMV–soybean pathosystem, and increases the understanding of the basis of the different disease responses of SMV strains.

Sign in / Sign up

Export Citation Format

Share Document