scholarly journals Elements Involved in the Rsv3-Mediated Extreme Resistance against an Avirulent Strain of Soybean Mosaic Virus

Viruses ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 581 ◽  
Author(s):  
Mazen Alazem ◽  
Kuan-Chieh Tseng ◽  
Wen-Chi Chang ◽  
Jang-Kyun Seo ◽  
Kook-Hyung Kim
Keyword(s):  
Mosaic Virus ◽  
Virulent Strain ◽  
Soybean Mosaic Virus ◽  
Avirulent Strain ◽  
Extreme Resistance ◽  
Rapid Induction ◽  
Soybean Plants ◽  
Acid Pathway ◽  
Rna Pathways ◽  
Si Rna

Extreme resistance (ER) is a type of R-gene-mediated resistance that rapidly induces a symptomless resistance phenotype, which is different from the phenotypical R-resistance manifested by the programmed cell death, accumulation of reactive oxygen species, and hypersensitive response. The Rsv3 gene in soybean cultivar L29 is responsible for ER against the avirulent strain G5H of soybean mosaic virus (SMV), but is ineffective against the virulent strain G7H. Rsv3-mediated ER is achieved through the rapid accumulation of callose, which arrests SMV-G5H at the point of infection. Callose accumulation, however, may not be the lone mechanism of this ER. Analyses of RNA-seq data obtained from infected soybean plants revealed a rapid induction of the abscisic acid pathway at 8 h post infection (hpi) in response to G5H but not to G7H, which resulted in the down-regulation of transcripts encoding β-1,3 glucanases that degrade callose in G5H-infected but not G7H-infected plants. In addition, parts of the autophagy and the small interfering (si) RNA pathways were temporally up-regulated at 24 hpi in response to G5H but not in response to G7H. The jasmonic acid (JA) pathway and many WRKY factors were clearly up-regulated only in G7H-infected plants. These results suggest that ER against SMV-G5H is achieved through the quick and temporary induction of ABA, autophagy, and the siRNA pathways, which rapidly eliminate G5H. The results also suggest that suppression of the JA pathway in the case of G5H is important for the Rsv3-mediated ER.

scholarly journals An Avirulent Strain of Soybean Mosaic Virus Reverses the Defensive Effect of Abscisic Acid in a Susceptible Soybean Cultivar

Viruses ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 879 ◽  
Author(s):  
Mazen Alazem ◽  
Kristin Widyasari ◽  
Kook-Hyung Kim
Keyword(s):  
Abscisic Acid ◽  
Mosaic Virus ◽  
Rna Silencing ◽  
Defense Mechanisms ◽  
Virulent Strain ◽  
Soybean Mosaic Virus ◽  
Resistance Mechanisms ◽  
Soybean Cultivar ◽  
Avirulent Strain ◽  
Rapid Induction

In soybean cultivar L29, the Rsv3 gene is responsible for extreme resistance (ER) against the soybean mosaic virus avirulent strain G5H, but is ineffective against the virulent strain G7H. Part of this ER is attributed to the rapid increase in abscisic acid (ABA) and callose, and to the rapid induction of several genes in the RNA-silencing pathway. Whether these two defense mechanisms are correlated or separated in the ER is unknown. Here, we found that ABA treatment of L29 plants increased the expression of several antiviral RNA-silencing genes as well as the PP2C3a gene, which was previously shown to increase callose accumulation; as a consequence, ABA increased the resistance of L29 plants to G7H. The effect of ABA treatment on these genes was weaker in the rsv3-null cultivar (Somyungkong) than in L29. Besides, G5H-infection of Somyungkong plants subverted the effect of ABA leading to reduced callose accumulation and decreased expression of several RNA-silencing genes, which resulted in increased susceptibility to G5H infection. ABA treatment, however, still induced some resistance to G7H in Somyungkong, but only AGO7b was significantly induced. Our data suggest that Rsv3 modulates the effect of ABA on these two resistance mechanisms, i.e., callose accumulation and the antiviral RNA-silencing pathway, and that in the absence of Rsv3, some strains can reverse the effect of ABA and thereby facilitate their replication and spread.

GmGSTU13 is related to the development of mosaic symptoms in soybean plants infected with Soybean mosaic virus

2021 ◽  
Author(s):  
Kai Zhang ◽  
Yingchao Shen ◽  
Tao Wang ◽  
Yu Wang ◽  
Song Xue ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Soybean Mosaic Virus ◽  
Positive Control ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
Protein Levels ◽  
Cp Gene ◽  
Viral Coat ◽  
Soybean Plants ◽  
Different Strains

The leaves of soybean cv. ZheA8901 show various symptoms (necrosis, mosaic and symptomless) when infected with different strains of Soybean mosaic virus (SMV). Based on a proteomic analysis performed with tandem mass tags (TMT), 736 proteins were differentially expressed from soybean samples that showed asymptomatic, mosaic and necrosis symptoms induced by SMV strains SC3, SC7, and SC15, respectively. Among these, GmGSTU13 and APX (ascorbate peroxidase) were only upregulated in mosaic and symptomless leaves, respectively. The protein level of GmGSTU13 determined by Western blot was consistent with TMT analysis, qRT-PCR analysis showed that GmGSTU13 mRNA levels in mosaic plants was 5.26- and 3.75-fold higher than that in necrotic and symptomless plants, respectively. Additionally, the expression of viral coat protein (CP) gene was increased, and serious mosaic symptoms were observed in GmGSTU13-overexpressing plants inoculated with all three SMV strains. These results showed that GmGSTU13 is associated with the development of SMV-induced mosaic symptoms in soybean and that APX is upregulated in symptomless leaves at both the transcriptional and protein levels. In APX gene-silenced soybean plants, the relative expression of the viral CP gene was 1.50, 7.59 and 1.30 times higher than in positive control plants inoculated with the three SMV strains, suggesting that the upregulation of APX may be associated with lack of symptoms in soybean infected with SMV. This work provides a useful dataset for identifying key proteins responsible for symptom development in soybean infected with different SMV strains.

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 Multiple Loci Condition Seed Transmission of Soybean mosaic virus (SMV) and SMV-Induced Seed Coat Mottling in Soybean

2011 ◽  
Vol 101 (6) ◽  
pp. 750-756 ◽  
Author(s):  
Leslie L. Domier ◽  
Houston A. Hobbs ◽  
Nancy K. McCoppin ◽  
Charles R. Bowen ◽  
Todd A. Steinlage ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Seed Coat ◽  
Soybean Mosaic Virus ◽  
Seed Transmission ◽  
Primary Sources ◽  
Posttranscriptional Gene Silencing ◽  
Plant Introductions ◽  
Multiple Loci ◽  
Soybean Plants ◽  
Simple Sequence

Infection of soybean plants with Soybean mosaic virus (SMV), which is transmitted by aphids and through seed, can cause significant reductions in seed production and quality. Because seedborne infections are the primary sources of inoculum for SMV infections in North America, host-plant resistance to seed transmission can limit the pool of plants that can serve as sources of inoculum. To examine the inheritance of SMV seed transmission in soybean, crosses were made between plant introductions (PIs) with high (PI88799), moderate (PI60279), and low (PI548391) rates of transmission of SMV through seed. In four F2 populations, SMV seed transmission segregated as if conditioned by two or more genes. Consequently, a recombinant inbred line population was derived from a cross between PIs 88799 and 548391 and evaluated for segregation of SMV seed transmission, seed coat mottling, and simple sequence repeat markers. Chromosomal regions on linkage groups C1 and C2 were significantly associated with both transmission of isolate SMV 413 through seed and SMV-induced seed coat mottling, and explained ≈42.8 and 46.4% of the variability in these two traits, respectively. Chromosomal regions associated with seed transmission and seed coat mottling contained homologues of Arabidopsis genes DCL3 and RDR6, which encode enzymes involved in RNA-mediated transcriptional and posttranscriptional gene silencing.

scholarly journals Occurrence of Seed Coat Mottling in Soybean Plants Inoculated with Bean pod mottle virus and Soybean mosaic virus

Plant Disease ◽  
2003 ◽  
Vol 87 (11) ◽  
pp. 1333-1336 ◽  
Author(s):  
H. A. Hobbs ◽  
G. L. Hartman ◽  
Y. Wang ◽  
C. B. Hill ◽  
R. L. Bernard ◽  
...  
Keyword(s):  
Virus Infection ◽  
Mosaic Virus ◽  
Resistance Gene ◽  
Seed Coat ◽  
Soybean Mosaic Virus ◽  
Soybean Seed ◽  
Mottle Virus ◽  
Bean Pod Mottle Virus ◽  
Soybean Plants ◽  
Soybean Seed Coat

Soybean seed coat mottling often has been a problematic symptom for soybean growers and the soybean industry. The percentages of seed in eight soybean lines with seed coat mottling were evaluated at harvest after inoculating plants during the growing season with Bean pod mottle virus (BPMV), Soybean mosaic virus (SMV), and both viruses inside an insect-proof cage in the field. Results from experiments conducted over 2 years indicated that plants infected with BPMV and SMV, alone or in combination, produced seed coat mottling, whereas noninoculated plants produced little or no mottled seed. BPMV and SMV inoculated on the same plants did not always result in higher percentages of mottled seed compared with BPMV or SMV alone. There was significant virus, line, and virus-line interaction for seed coat mottling. The non-seed-coat-mottling gene (Im) in Williams isoline L77-5632 provided limited, if any, protection against mottling caused by SMV and none against BPMV. The Peanut mottle virus resistance gene Rpv1 in Williams isoline L85-2308 did not give any protection against mottling caused by SMV, whereas the SMV resistance gene Rsv1 in Williams isoline L78-379 and the resistance gene or genes in the small-seeded line L97-946 gave high levels of protection against mottling caused by SMV. The correlations (r = 0.77 for year 2000 and r = 0.89 for year 2001) between virus infection of the parent plant and seed coat mottling were significant (P = 0.01), indicating that virus infection of plants caused seed coat mottling.

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 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.

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