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 Involvement of the P1 Cistron in Overcoming eIF4E-Mediated Recessive Resistance Against Clover yellow vein virus in Pea

2010 ◽  
Vol 23 (11) ◽  
pp. 1460-1469 ◽  
Author(s):  
Kenji S. Nakahara ◽  
Ryoko Shimada ◽  
Sun-Hee Choi ◽  
Haruko Yamamoto ◽  
Jun Shao ◽  
...  
Keyword(s):  
Systemic Infection ◽  
Translation Initiation Factor ◽  
Yellow Vein ◽  
Initiation Factor ◽  
Recessive Resistance ◽  
Nonsynonymous Mutation ◽  
Eukaryotic Translation ◽  
Clover Yellow Vein Virus ◽  
Recessive Genes ◽  
Eukaryotic Translation Initiation

Two recessive genes (cyv1 and cyv2) are known to confer resistance against Clover yellow vein virus (ClYVV) in pea. cyv2 has recently been revealed to encode eukaryotic translation initiation factor 4E (eIF4E) and is the same allele as sbm1 and wlm against other potyviruses. Although mechanical inoculation with crude sap is rarely able to cause infection of a cyv2 pea, biolistic inoculation of the infectious ClYVV cDNA clone does. At the infection foci, the breaking virus frequently emerges, resulting in systemic infection. Here, a derived cleaved-amplified polymorphic sequence analysis showed that the breakings were associated with a single nonsynonymous mutation on the ClYVV genome, corresponding to an amino-acid substitution at position 24 (isoleucine to valine) on the P1 cistron. ClYVV with the point mutation was able to break the resistance. This is a first report demonstrating that P1 is involved in eIF4E-mediated recessive resistance.

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.

scholarly journals Activation of the Salicylic Acid Signaling Pathway Enhances Clover yellow vein virus Virulence in Susceptible Pea Cultivars

2009 ◽  
Vol 22 (2) ◽  
pp. 166-175 ◽  
Author(s):  
Go Atsumi ◽  
Uiko Kagaya ◽  
Hiroaki Kitazawa ◽  
Kenji Suto Nakahara ◽  
Ichiro Uyeda
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Mosaic Virus ◽  
Signaling Pathway ◽  
Dominant Gene ◽  
Plant Introduction ◽  
Yellow Vein ◽  
Yellow Mosaic Virus ◽  
Clover Yellow Vein Virus ◽  
Sa Signaling

The wild-type strain (Cl-WT) of Clover yellow vein virus (ClYVV) systemically induces cell death in pea cv. Plant introduction (PI) 118501 but not in PI 226564. A single incompletely dominant gene, Cyn1, controls systemic cell death in PI 118501. Here, we show that activation of the salicylic acid (SA) signaling pathway enhances ClYVV virulence in susceptible pea cultivars. The kinetics of virus accumulation was not significantly different between PI 118501 (Cyn1) and PI 226564 (cyn1); however, the SA-responsive chitinase gene (SA-CHI) and the hypersensitive response (HR)-related gene homologous to tobacco HSR203J were induced only in PI 118501 (Cyn1). Two mutant viruses with mutations in P1/HCPro, which is an RNA-silencing suppressor, reduced the ability to induce cell death and SA-CHI expression. The application of SA and of its analog benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester (BTH) partially complemented the reduced virulence of mutant viruses. These results suggest that high activation of the SA signaling pathway is required for ClYVV virulence. Interestingly, BTH could enhance Cl-WT symptoms in PI 226564 (cyn1). However, it could not enhance symptoms induced by White clover mosaic virus and Bean yellow mosaic virus. Our report suggests that the SA signaling pathway has opposing functions in compatible interactions, depending on the virus–host combination.

scholarly journals Quantitative and Qualitative Involvement of P3N-PIPO in Overcoming Recessive Resistance against Clover Yellow Vein Virus in Pea Carrying the cyv1 Gene

2013 ◽  
Vol 87 (13) ◽  
pp. 7326-7337 ◽  
Author(s):  
S. H. Choi ◽  
Y. Hagiwara-Komoda ◽  
K. S. Nakahara ◽  
G. Atsumi ◽  
R. Shimada ◽  
...  
Keyword(s):  
Yellow Vein ◽  
Recessive Resistance ◽  
Clover Yellow Vein Virus

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 RIPK3-Dependent Recruitment of Low-Inflammatory Myeloid Cells Does Not Protect from Systemic Salmonella Infection

mBio ◽  
2020 ◽  
Vol 11 (5) ◽  
Author(s):  
John Satkovich ◽  
Christopher J. Anderson ◽  
Christopher B. Medina ◽  
Matteo Ottolini ◽  
John R. Lukens ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Myeloid Cells ◽  
Systemic Infection ◽  
Intracellular Pathogen ◽  
Bacterial Gene ◽  
Content Type ◽  
Regulated Cell Death ◽  
Caspase Inhibition

ABSTRACT Regulated macrophage death has emerged as an important mechanism to defend against intracellular pathogens. However, the importance and consequences of macrophage death during bacterial infection are poorly resolved. This is especially true for the recently described RIPK3-dependent lytic cell death, termed necroptosis. Salmonella enterica serovar Typhimurium is an intracellular pathogen that precisely regulates virulence expression within macrophages to evade and manipulate immune responses, which is a key factor in its ability to cause severe systemic infections. We combined genetic and pharmacological approaches to examine the importance of RIPK3 for S. Typhimurium-induced macrophage death using conditions that recapitulate bacterial gene expression during systemic infection in vivo. Our findings indicate that noninvasive S. Typhimurium does not naturally induce macrophage necroptosis but does so in the presence of pan-caspase inhibition. Moreover, our data suggest that RIPK3 induction (following caspase inhibition) does not impact host survival following S. Typhimurium infection, which differs from previous findings based on inert lipopolysaccharide (LPS) injections. Finally, although necroptosis is typically characterized as highly inflammatory, our data suggest that RIPK3 skews the peritoneal myeloid population away from an inflammatory profile to that of a classically noninflammatory profile. Collectively, these data improve our understanding of S. Typhimurium-macrophage interactions, highlight the possibility that purified bacterial components may not accurately recapitulate the complexity of host-pathogen interactions, and reveal a potential and unexpected role for RIPK3 in resolving inflammation. IMPORTANCE Macrophages employ multiple strategies to limit pathogen infection. For example, macrophages may undergo regulated cell death, including RIPK3-dependent necroptosis, as a means of combatting intracellular bacterial pathogens. However, bacteria have evolved mechanisms to evade or exploit immune responses. Salmonella is an intracellular pathogen that avoids and manipulates immune detection within macrophages. We examined the contribution of RIPK3 to Salmonella-induced macrophage death. Our findings indicate that noninvasive Salmonella does not naturally induce necroptosis, but it does so when caspases are inhibited. Moreover, RIPK3 induction (following caspase inhibition) does not impact host survival following Salmonella systemic infection. Finally, our data show that RIPK3 induction results in recruitment of low-inflammatory myeloid cells, which was unexpected, as necroptosis is typically described as highly inflammatory. Collectively, these data improve our understanding of pathogen-macrophage interactions, including outcomes of regulated cell death during infection in vivo, and reveal a potential new role for RIPK3 in resolving inflammation.

Antecedents and consequences of replacing international independent intermediaries

2014 ◽  
Vol 26 (3) ◽  
pp. 218-237
Author(s):  
Erik B. Nes
Keyword(s):  
Longitudinal Design ◽  
Operation Mode ◽  
Content Type ◽  
Performance Variables ◽  
Direct Sales ◽  
Home Based ◽  
Process Theories ◽  
Antecedents And Consequences ◽  
Communication Control ◽  
And Control

Purpose – What characterizes the relationships with intermediaries that are soon to be replaced, and are the replacements successful? The paper aims to discuss these issues. Design/methodology/approach – The study applies a longitudinal design. The paper conducted a survey among a sample of exporters concerning their relationships with independent intermediaries in terms of trust, commitment, communication, control and two performance variables; financial performance and strategic goal achievement. Five years thereafter the author contacted the same companies again and questioned which independent intermediaries had been replaced in the period. The author then compared the replaced intermediaries with the extended intermediaries before they were replaced and analysed changes in the evaluations of the relationships and of the performance after the replacement. Findings – The relationships with terminated intermediaries that were replaced by sales subsidiary or home-based direct sales were characterized having higher trust, communication and control than extended relationships before replacement. While it may be surprising that these quite successful relationships were terminated, this is in line with internationalization process theories. The replacements, both intermediaries that were replaced by other intermediaries and by sales subsidiary/home-based direct sales, were highly successful in terms of improvement in performance and behavioural relationship variables. Research limitations/implications – The empirical findings are limited by the sample and by data collection from the principal only in the dyadic relations. Practical implications – International independent intermediaries should analyse the likelihood of being replaced by the principal because the relationship or the performance is unsatisfactory, but also because of satisfactory evaluations. Terminations of satisfactory relationships tend to be accompanied by change in operation mode to internal organization. The independent intermediary should in such cases build a defence structure against unwanted termination and/or prepare for buyout. The success of the replacements suggests that international marketers benefit from being proactive in replacing intermediaries with new intermediaries or with a hierarchal entry mode. Originality/value – This is the first study that applies most of these variables from interorganizational relations theory in the study of international independent intermediary replacements. It is also the first to give insight into the consequences of intermediary terminations.

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