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

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.

2021 ◽  
Author(s):  
Bowen Li ◽  
Adhimoolam Karthikeyan ◽  
Liqun Wang ◽  
Jinlong Yin ◽  
Tongtong Jin ◽  
...  

Abstract Background: Soybean mosaic virus (SMV) is the most devastating pathogen of soybean. MicroRNAs (miRNAs) are a class of non-coding RNAs (21-24 nucleotides) and play important roles in regulating defense responses against pathogens. However, miRNA's response to SMV in soybean is not as well documented. Result: In this study, we analyzed 18 miRNA libraries, including three biological replicates from two soybean lines (Resistant and susceptible lines to SMV strain SC3 selected from the near-isogenic lines of Qihuang No. 1× Nannong1138-2) after virus infection at three different time intervals (0 dpi, 7 dpi, and 14 dpi). A total of 1,092 miRNAs, including 608 known miRNAs and 484 novel miRNAs were detected. Differential expression analyses identified the miRNAs responded during soybean-SMV interaction. Then, miRNAs potential target genes were predicted via data mining, and functional annotation was done by Gene Ontology (GO) analysis. Eventually, the expression patterns of several miRNAs validated by quantitative real-time PCR analysis are consistent with sequencing results. Conclusion: We have identified a large number of miRNAs and their target genes and also functional annotations. Our study provides additional information on soybean miRNAs and an insight into the role of miRNAs during SMV-infection in soybean.


2013 ◽  
Vol 26 (2) ◽  
pp. 203-215 ◽  
Author(s):  
R.-H. Wen ◽  
B. Khatabi ◽  
T. Ashfield ◽  
M. A. Saghai Maroof ◽  
M. R. Hajimorad

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.


2020 ◽  
Vol 71 (5) ◽  
pp. 477
Author(s):  
Hexiang Luan ◽  
Yongkun Zhong ◽  
Dagang Wang ◽  
Rui Ren ◽  
Le Gao ◽  
...  

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.


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

2008 ◽  
Vol 21 (7) ◽  
pp. 937-946 ◽  
Author(s):  
M. R. Hajimorad ◽  
A. L. Eggenberger ◽  
J. H. Hill

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.


2008 ◽  
Vol 21 (7) ◽  
pp. 931-936 ◽  
Author(s):  
A. L. Eggenberger ◽  
M. R. Hajimorad ◽  
J. H. Hill

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.


2009 ◽  
Vol 22 (9) ◽  
pp. 1151-1159 ◽  
Author(s):  
Jang-Kyun Seo ◽  
Suk-Ha Lee ◽  
Kook-Hyung Kim

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.


2020 ◽  
Vol 38 (4) ◽  
pp. 666-675
Author(s):  
Qinghua Yang ◽  
Hangxia Jin ◽  
Xiaomin Yu ◽  
Xujun Fu ◽  
Haijian Zhi ◽  
...  

2009 ◽  
Vol 20 (9) ◽  
pp. 2389-2400 ◽  
Author(s):  
Adnane Sellam ◽  
Christopher Askew ◽  
Elias Epp ◽  
Hugo Lavoie ◽  
Malcolm Whiteway ◽  
...  

The SAGA/ADA coactivator complex, which regulates numerous cellular processes by coordinating histone acetylation, is widely conserved throughout eukaryotes, and analysis of the Candida albicans genome identifies the components of this complex in the fungal pathogen. We investigated the multiple functions of SAGA/ADA in C. albicans by determining the genome-wide occupancy of Ada2p using chromatin immunoprecipitation (ChIP). Ada2p is recruited to 200 promoters upstream of genes involved in different stress-response functions and metabolic processes. Phenotypic and transcriptomic analysis of ada2 mutant showed that Ada2p is required for the responses to oxidative stress, as well as to treatments with tunicamycin and fluconazole. Ada2p recruitment to the promoters of oxidative resistance genes is mediated by the transcription factor Cap1p, and coactivator function were also established for Gal4p, which recruits Ada2p to the promoters of glycolysis and pyruvate metabolism genes. Cooccupancy of Ada2p and the drug resistance regulator Mrr1p on the promoters of core resistance genes characterizing drug resistance in clinical strains was also demonstrated. Ada2p recruitment to the promoters of these genes were shown to be completely dependent on Mrr1p. Furthermore, ADA2 deletion causes a decrease in H3K9 acetylation levels of target genes, thus illustrating its importance for histone acetyl transferase activity.


2000 ◽  
Vol 13 (11) ◽  
pp. 1266-1270 ◽  
Author(s):  
Candace Whitmer Collmer ◽  
Marcia Fisher Marston ◽  
Jessica C. Taylor ◽  
Molly Jahn

The resistance to the potyvirus Bean common mosaic virus (BCMV) conferred by the I allele in cultivars of Phaseolus vulgaris has been characterized as dominant, and it has been associated with both immunity and a systemic vascular necrosis in infected bean plants under field, as well as controlled, conditions. In our attempts to understand more fully the nature of the interaction between bean with the I resistance allele and the pathogen BCMV, we carefully varied both I allele dosage and temperature and observed the resulting, varying resistance responses. We report here that the I allele in the bean cultivars we studied is not dominant, but rather incompletely dominant, and that the system can be manipulated to show in plants a continuum of response to BCMV that ranges from immunity or extreme resistance, to hypersensitive resistance, to systemic phloem necrosis (and subsequent plant death). We propose that the particular phenotypic outcome in bean results from a quantitative interaction between viral pathogen and plant host that can be altered to favor one or the other by manipulating I allele dosage, temperature, viral pathogen, or plant cultivar.


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