scholarly journals Temperature-Dependent Wsm1 and Wsm2 Gene-Specific Blockage of Viral Long-Distance Transport Provides Resistance to Wheat streak mosaic virus and Triticum mosaic virus in Wheat

2016 ◽  
Vol 29 (9) ◽  
pp. 724-738 ◽  
Author(s):  
Satyanarayana Tatineni ◽  
Everlyne N. Wosula ◽  
Melissa Bartels ◽  
Gary L. Hein ◽  
Robert A. Graybosch

Wheat streak mosaic virus (WSMV) and Triticum mosaic virus (TriMV) are economically important viral pathogens of wheat. Wheat cvs. Mace, carrying the Wsm1 gene, is resistant to WSMV and TriMV, and Snowmass, with Wsm2, is resistant to WSMV. Viral resistance in both cultivars is temperature sensitive and is effective at 18°C or below but not at higher temperatures. The underlying mechanisms of viral resistance of Wsm1 and Wsm2, nonallelic single dominant genes, are not known. In this study, we found that fluorescent protein–tagged WSMV and TriMV elicited foci that were approximately similar in number and size at 18 and 24°C, on inoculated leaves of resistant and susceptible wheat cultivars. These data suggest that resistant wheat cultivars at 18°C facilitated efficient cell-to-cell movement. Additionally, WSMV and TriMV efficiently replicated in inoculated leaves of resistant wheat cultivars at 18°C but failed to establish systemic infection, suggesting that Wsm1- and Wsm2-mediated resistance debilitated viral long-distance transport. Furthermore, we found that neither virus was able to enter the leaf sheaths of inoculated leaves or crowns of resistant wheat cultivars at 18°C but both were able to do so at 24°C. Thus, wheat cvs. Mace and Snowmass provide resistance at the long-distance movement stage by specifically blocking virus entry into the vasculature. Taken together, these data suggest that both Wsm1 and Wsm2 genes similarly confer virus resistance by temperature-dependent impairment of viral long-distance movement.

2014 ◽  
Vol 27 (2) ◽  
pp. 150-162 ◽  
Author(s):  
Satyanarayana Tatineni ◽  
Roy French

Viral determinants and mechanisms involved in extension of host range of monocot-infecting viruses are poorly understood. Viral coat proteins (CP) serve many functions in almost every aspect of the virus life cycle. The role of the C-terminal region of Wheat streak mosaic virus (WSMV) CP in virus biology was examined by mutating six negatively charged aspartic acid residues at positions 216, 289, 290, 326, 333, and 334. All of these amino acid residues are dispensable for virion assembly, and aspartic acid residues at positions 216, 333, and 334 are expendable for normal infection of wheat and maize. However, mutants D289N, D289A, D290A, DD289/290NA, and D326A exhibited slow cell-to-cell movement in wheat, which resulted in delayed onset of systemic infection, followed by a rapid recovery of genomic RNA accumulation and symptom development. Mutants D289N, D289A, and D326A inefficiently infected maize, eliciting milder symptoms, while D290A and DD289/290NA failed to infect systemically, suggesting that the C-terminus of CP is involved in differential infection of wheat and maize. Mutation of aspartic acid residues at amino acid positions 289, 290, and 326 severely debilitated virus ingress into the vascular system of maize but not wheat, suggesting that these amino acids facilitate expansion of WSMV host range through host-specific long-distance transport.


2019 ◽  
Vol 32 (3) ◽  
pp. 336-350 ◽  
Author(s):  
Satyanarayana Tatineni ◽  
Jeff Alexander ◽  
Adarsh K. Gupta ◽  
Roy French

Wheat streak mosaic virus (WSMV) and Triticum mosaic virus (TriMV), distinct members in the family Potyviridae, are economically important wheat-infecting viruses in the Great Plains region. Previously, we reported that coinfection of wheat by WSMV and TriMV caused disease synergism with increased concentration of both viruses. The mechanisms of synergistic interaction between WSMV and TriMV and the effects of prior infection of wheat by either of these “synergistically interacting partner” (SIP) viruses on the establishment of local and systemic infection by the other SIP virus are not known. In this study, using fluorescent protein-tagged viruses, we found that prior infection of wheat by WSMV or TriMV negatively affected the onset and size of local foci elicited by subsequent SIP virus infection compared with those in buffer-inoculated wheat. These data revealed that prior infection of wheat by an SIP virus has no measurable advantage for another SIP virus on the initiation of infection and cell-to-cell movement. In TriMV-infected wheat, WSMV exhibited accelerated long-distance movement and increased accumulation of genomic RNAs compared with those in buffer-inoculated wheat, indicating that TriMV-encoded proteins complemented WSMV for efficient systemic infection. In contrast, TriMV displayed delayed systemic infection in WSMV-infected wheat, with fewer genomic RNA copies in early stages of infection compared with those in buffer-inoculated wheat. However, during late stages of infection, TriMV accumulation in WSMV-infected wheat increased rapidly with accelerated long-distance movement compared with those in buffer-inoculated wheat. Taken together, these data suggest that interactions between synergistically interacting WSMV and TriMV are asymmetrical; thus, successful establishment of synergistic interaction between unrelated viruses will depend on the order of infection of plants by SIP viruses.


2005 ◽  
Vol 16 (11) ◽  
pp. 5191-5201 ◽  
Author(s):  
Isabel Schuchardt ◽  
Daniela Aßmann ◽  
Eckhard Thines ◽  
Christian Schuberth ◽  
Gero Steinberg

Long-distance transport is crucial for polar-growing cells, such as neurons and fungal hyphae. Kinesins and myosins participate in this process, but their functional interplay is poorly understood. Here, we investigate the role of kinesin motors in hyphal growth of the plant pathogen Ustilago maydis. Although the microtubule plus-ends are directed to the hyphal tip, of all 10 kinesins analyzed, only conventional kinesin (Kinesin-1) and Unc104/Kif1A-like kinesin (Kinesin-3) were up-regulated in hyphae and they are essential for extended hyphal growth. Δkin1 and Δkin3 mutant hyphae grew irregular and remained short, but they were still able to grow polarized. No additional phenotype was detected in Δkin1rkin3 double mutants, but polarity was lost in Δmyo5rkin1 and Δmyo5rkin3 mutant cells, suggesting that kinesins and class V myosin cooperate in hyphal growth. Consistent with such a role in secretion, fusion proteins of green fluorescent protein and Kinesin-1, Myosin-V, and Kinesin-3 accumulate in the apex of hyphae, a region where secretory vesicles cluster to form the fungal Spitzenkörper. Quantitative assays revealed a role of Kin3 in secretion of acid phosphatase, whereas Kin1 was not involved. Our data demonstrate that just two kinesins and at least one myosin support hyphal growth.


2014 ◽  
Vol 95 (2) ◽  
pp. 496-505 ◽  
Author(s):  
Clémence Hipper ◽  
Baptiste Monsion ◽  
Diane Bortolamiol-Bécet ◽  
Véronique Ziegler-Graff ◽  
Véronique Brault

Viral genomic RNA of the Turnip yellows virus (TuYV; genus Polerovirus; family Luteoviridae) is protected in virions formed by the major capsid protein (CP) and the minor component, the readthrough (RT*) protein. Long-distance transport, used commonly by viruses to systemically infect host plants, occurs in phloem sieve elements and two viral forms of transport have been described: virions and ribonucleoprotein (RNP) complexes. With regard to poleroviruses, virions have always been presumed to be the long-distance transport form, but the potential role of RNP complexes has not been investigated. Here, we examined the requirement of virions for polerovirus systemic movement by analysing CP-targeted mutants that were unable to form viral particles. We confirmed that TuYV mutants that cannot encapsidate into virions are not able to reach systemic leaves. To completely discard the possibility that the introduced mutations in CP simply blocked the formation or the movement of RNP complexes, we tested in trans complementation of TuYV CP mutants by providing WT CP expressed in transgenic plants. WT CP was able to facilitate systemic movement of TuYV CP mutants and this observation was always correlated with the formation of virions. This demonstrated clearly that virus particles are essential for polerovirus systemic movement.


2019 ◽  
Vol 32 (11) ◽  
pp. 1475-1486 ◽  
Author(s):  
Yuki Matsuo ◽  
Fawzia Novianti ◽  
Miki Takehara ◽  
Toshiyuki Fukuhara ◽  
Tsutomu Arie ◽  
...  

Plant activators, including acibenzolar-S-methyl (ASM), are chemical compounds that stimulate plant defense responses to pathogens. ASM treatment inhibits infection by a variety of plant viruses, however, the mechanisms of this broad-spectrum and strong effect remain poorly understood. We employed green fluorescent protein (GFP)-expressing viruses and Nicotiana benthamiana plants to identify the infection stages that are restricted by ASM. ASM suppressed infection by three viral species, plantago asiatica mosaic virus (PlAMV), potato virus X (PVX), and turnip mosaic virus (TuMV), in inoculated cells. Furthermore, ASM delayed the long-distance movement of PlAMV and PVX, and the cell-to-cell (short range) movement of TuMV. The ASM-mediated delay of long-distance movement of PlAMV was not due to the suppression of viral accumulation in the inoculated leaves, indicating that ASM restricts PlAMV infection in at least two independent steps. We used Arabidopsis thaliana mutants to show that the ASM-mediated restriction of PlAMV infection requires the NPR1 gene but was independent of the dicer-like genes essential for RNA silencing. Furthermore, experiments using protoplasts showed that ASM treatment inhibited PlAMV replication without cell death. Our approach, using GFP-expressing viruses, will be useful for the analysis of mechanisms underlying plant activator–mediated virus restriction.


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