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.

Occurrence of bean yellow mosaic virus in subterranean clover pastures and perennial native legumes

1994 ◽  
Vol 45 (1) ◽  
pp. 183 ◽  
Author(s):  
SJ McKirdy ◽  
BA Coutts ◽  
RAC Jones
Keyword(s):  
Mosaic Virus ◽  
Western Australia ◽  
White Clover ◽  
Subterranean Clover ◽  
Trifolium Subterraneum ◽  
Bean Yellow Mosaic Virus ◽  
Yellow Vein ◽  
Yellow Mosaic Virus ◽  
South West ◽  
Clover Yellow Vein Virus

In 1990, infection with bean yellow mosaic virus (BYMV) was widespread in subterranean clover (Trifolium subterraneum) pastures in the south-west of Western Australia. When 100 leaves were sampled at random per pasture, the virus was detected by ELISA in 23 of 87 pastures and incidences of infection ranged from 1 to 64%. BYMV was present in all seven districts surveyed, but highest incidences of infection occurred in the Busselton district. In smaller surveys in 1989 and 1992, incidences of infection in pastures were higher than in 1990, and ranged up to 90%. In 1992, when petals from 1703 samples of 59 species of perennial native legumes from 117 sites were tested by ELISA, only 1% were found infected with BYMV. The infected samples came from 5/7 districts surveyed. Species found infected were Kennedia prostrata, K. coccinea, Hovea elliptica and H. pungens. Representative isolates of BYMV from subterranean clover and native legumes did not infect white clover systemically confirming that clover yellow vein virus (CYVV) was not involved. It was concluded that BYMV infection was present in many subterranean clover pastures, but normally at low incidences, except in epidemic years such as 1992. Also, perennial native legumes are unlikely to act as major reservoirs for reinfection of annual pastures each year. In areas of Australia with Mediterranean climates where perennial pastures are absent, persistence of the virus over summer is therefore by some other method than infection of perennials.

scholarly journals Cross-Protection Against Bean yellow mosaic virus (BYMV) and Clover yellow vein virus by Attenuated BYMV Isolate M11

2009 ◽  
Vol 99 (3) ◽  
pp. 251-257 ◽  
Author(s):  
Eiko Nakazono-Nagaoka ◽  
Tsubasa Takahashi ◽  
Takumi Shimizu ◽  
Yoshitaka Kosaka ◽  
Tomohide Natsuaki ◽  
...  
Keyword(s):  
Amino Acid ◽  
Mosaic Virus ◽  
Phylogenetic Trees ◽  
Amino Acid Sequences ◽  
Cross Protection ◽  
Bean Yellow Mosaic Virus ◽  
Yellow Vein ◽  
Yellow Mosaic Virus ◽  
Challenge Virus ◽  
Clover Yellow Vein Virus

Attenuated isolate M11 of Bean yellow mosaic virus (BYMV), obtained after exposing BYMV-infected plants to low temperature, and its efficacy in cross-protecting against infection by BYMV isolates from gladiolus, broad bean (Vicia faba) and white clover (Trifolium repens) was assessed with western blotting and reverse transcription-polymerase chain reaction. The level of cross-protection varied depending on the challenge virus isolates. Cross-protection was complete against BYMV isolates from gladiolus, but incomplete against BYMV isolates from other hosts. M11 also partially cross-protected against an isolate of Clover yellow vein virus. A comparison of the nucleotide sequence of M11 and those of BYMV isolates from gladiolus and from other hosts showed higher homology among gladiolus isolates than the homology between gladiolus isolates and nongladiolus isolates. In the phylogenetic trees, constructed using the nucleotide sequences of an overall polyprotein of the genomes, five gladiolus isolates clustered together, completely separated from the three BYMV isolates from other hosts. A comparison of the amino acid sequences between M11 and its parental isolate IbG, and analysis of recombinant infectious clones between M11 and IbG revealed that an amino acid at position 314 was involved in the attenuation of BYMV.

scholarly journals Restoration of Defective Cross Talk in ssi2 Mutants: Role of Salicylic Acid, Jasmonic Acid, and Fatty Acids in SSI2-Mediated Signaling

2003 ◽  
Vol 16 (11) ◽  
pp. 1022-1029 ◽  
Author(s):  
Pradeep Kachroo ◽  
Aardra Kachroo ◽  
Ludmila Lapchyk ◽  
David Hildebrand ◽  
Daniel F. Klessig
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Jasmonic Acid ◽  
Cross Talk ◽  
Pr Genes ◽  
Exogenous Application ◽  
Basal Level Expression ◽  
Sa Signaling ◽  
Spontaneous Cell Death

The Arabidopsis mutants ssi2 and fab2 are defective in stearoyl ACP desaturase, which causes altered salicylic acid (SA)- and jasmonic acid (JA)-mediated defense signaling. Both ssi2 and fab2 plants show spontaneous cell death, express PR genes constitutively, accumulate high levels of SA, and exhibit enhanced resistance to bacterial and oomycete pathogens. In contrast to constitutive activation of the SA pathway, ssi2 and fab2 plants are repressed in JA-mediated induction of the PDF1.2 gene, which suggests that the SSI2-mediated signaling pathway modulates cross talk between the SA and JA pathways. In this study, we have characterized two recessive nonallelic mutants in the ssi2 background, designated as rdc (restorer of defective cross talk) 2 and rdc8. Both ssi2 rdc mutants are suppressed in constitutive SA signaling, show basal level expression of PR-1 gene, and induce high levels of PDF1.2 in response to exogenous application of JA. Interestingly, while the rdc8 mutation completely abolishes spontaneous cell death in ssi2 rdc8 plants, the ssi2 rdc2 plants continue to show some albeit reduced cell death. Fatty acid (FA) analysis showed a reduction in 16:3 levels in ssi2 rdc8 plants, which suggests that this mutation may limit the flux of FAs into the pro-karyotic pathway of glycerolipid biosynthesis. Both rdc2 and rdc8 continue to accumulate high levels of 18:0, which suggests that 18:0 levels were responsible for neither constitutive SA signaling nor repression of JA-induced expression of the PDF1.2 gene in ssi2 plants. We also analyzed SA and JA responses of the fab2-derived shs1 mutant, which accumulates levels of 18:0 over 50% lower than those in the fab2 plants. Even though fab2 shs1 plants were morphologically bigger than fab2 plants, they expressed PR genes constitutively, showed HR-like cell death, and accumulated elevated levels of SA. However, unlike the ssi2 rdc plants, fab2 shs1 plants were unable to induce high levels of PDF1.2 expression in response to exogenous application of JA. Together, these results show that defective cross talk in ssi2 can be restored by second site mutations and is independent of morphological size of the plants, cell death, and elevated levels of 18:0.

scholarly journals A salivary effector enables whitefly to feed on host plants by eliciting salicylic acid-signaling pathway

2018 ◽  
Vol 116 (2) ◽  
pp. 490-495 ◽  
Author(s):  
Hong-Xing Xu ◽  
Li-Xin Qian ◽  
Xing-Wei Wang ◽  
Ruo-Xuan Shao ◽  
Yue Hong ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Signaling Pathway ◽  
Host Plants ◽  
Salivary Protein ◽  
In Planta ◽  
Protein Protein Interaction ◽  
Salicylic Acid Signaling ◽  
Homeobox Transcription Factor ◽  
Phloem Feeding ◽  
Sa Signaling

Phloem-feeding insects feed on plant phloem using their stylets. While ingesting phloem sap, these insects secrete saliva to circumvent plant defenses. Previous studies have shown that, to facilitate their feeding, many phloem-feeding insects can elicit the salicylic acid- (SA-) signaling pathway and thus suppress effective jasmonic acid defenses. However, the molecular basis for the regulation of the plant's defense by phloem-feeding insects remains largely unknown. Here, we show that Bt56, a whitefly-secreted low molecular weight salivary protein, is highly expressed in the whitefly primary salivary gland and is delivered into host plants during feeding. Overexpression of the Bt56 gene in planta promotes susceptibility of tobacco to the whitefly and elicits the SA-signaling pathway. In contrast, silencing the whitefly Bt56 gene significantly decreases whitefly performance on host plants and interrupts whitefly phloem feeding with whiteflies losing the ability to activate the SA pathway. Protein-protein interaction assays show that the Bt56 protein directly interacts with a tobacco KNOTTED 1-like homeobox transcription factor that decreases whitefly performance and suppresses whitefly-induced SA accumulation. The Bt56 orthologous genes are highly conserved but differentially expressed in different species of whiteflies. In conclusion, Bt56 is a key salivary effector that promotes whitefly performance by eliciting salicylic acid-signaling pathway.

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