scholarly journals Lower temperature influences Cauliflower mosaic virus systemic infection

2021 ◽  
Author(s):  
Roberto Alers-Velazquez ◽  
Sushant Khandekar ◽  
Clare Muller ◽  
Jennifer Boldt ◽  
Scott Leisner
Keyword(s):  
Nucleic Acid ◽  
Actin Cytoskeleton ◽  
Mosaic Virus ◽  
Virus Particle ◽  
Systemic Infection ◽  
Cauliflower Mosaic Virus ◽  
Particle Release ◽  
Systemic Symptoms ◽  
Lower Temperature ◽  
Temperature Exposure

AbstractLower temperatures delayed development of systemic symptoms by Cauliflower mosaic virus (CaMV) in two different plant hosts. However, lower temperature exposure increased CaMV nucleic acid levels in leaves of systemically-infected turnips. Furthermore, lower temperature altered the formation of aggregates formed by the CaMV major inclusion body (IB) protein, P6. Finally, lower temperature altered the architecture of the actin cytoskeleton. These data may suggest that lower temperatures alter the actin cytoskeleton, facilitating the formation of larger IBs that hold on to their internal virions more strongly than small ones, impairing virus particle release and causing a delay in systemic infection.

scholarly journals Multiple Domains Within the Cauliflower mosaic virus Gene VI Product Interact with the Full-Length Protein

2002 ◽  
Vol 15 (10) ◽  
pp. 1050-1057 ◽  
Author(s):  
Yongzhong Li ◽  
Scott M. Leisner
Keyword(s):  
Mosaic Virus ◽  
Systemic Infection ◽  
Full Length ◽  
Cauliflower Mosaic Virus ◽  
The Other ◽  
Multifunctional Protein ◽  
Viral Propagation ◽  
Self Association ◽  
Multiple Domains ◽  
Two Hybrid

The Cauliflower mosaic virus (CaMV) gene VI product (P6) is a multifunctional protein essential for viral propagation. It is likely that at least some of these functions require P6 self-association. The work described here was performed to confirm that P6 self-associates and to identify domains involved in this interaction. Yeast two-hybrid analyses indicated that full-length P6 self-associates and that this interaction is specific. Additional analyses indicated that at least four independent domains bind to full-length P6. When a central domain (termed domain D3) was removed, these interactions were abolished. However, this deleted P6 was able to bind to the full-length wild-type protein and to isolated domain D3. Viruses lacking domain D3 were incapable of producing a systemic infection. Isolated domain D3 was capable of binding to at least two of the other domains but was unable to self-associate. This suggests that domain D3 facilitates P6 self-association by binding to the other domains but not itself. The presence of multiple domains involved in P6 self-association may help explain the ability of this protein to form the intracellular inclusions characteristic of caulimoviruses.

scholarly journals Evaluation of ‘AU-Performance’ Watermelon for Its Response to Virus Inoculation

2009 ◽  
Vol 19 (3) ◽  
pp. 609-612 ◽  
Author(s):  
John F. Murphy ◽  
Fenny Dane
Keyword(s):  
Mosaic Virus ◽  
Fungal Pathogens ◽  
Citrullus Lanatus ◽  
Zucchini Yellow Mosaic Virus ◽  
Systemic Infection ◽  
Yellow Mosaic Virus ◽  
Watermelon Mosaic Virus ◽  
Susceptible Parent ◽  
Resistant Parent ◽  
Systemic Symptoms

The watermelon (Citrullus lanatus var. lanatus) ‘AU-Performance’ was developed for resistance to multiple fungal pathogens and the plant virus, zucchini yellow mosaic virus (ZYMV). A greenhouse-based evaluation was carried out to determine the response of ‘AU-Performance’ to inoculation with three important cucurbit (Cucurbitaceae) viruses in the genus Potyvirus: papaya ringspot virus (PRSV), watermelon mosaic virus (WMV), and ZYMV. The evaluation included the resistant parent (PI595203), the susceptible parent (‘AU-Producer’), and varieties AU-Allsweet and Charleston Gray. Each of the three viruses systemically infected ‘AU-Performance’ with 100% infection and development of characteristic systemic symptoms. The susceptible parent (‘AU-Producer’), ‘AU-Allsweet’, and ‘Charleston Gray’ responded similarly with 100% infection and systemic symptoms. In contrast, the resistant parent (PI595203) was resistant to WMV and ZYMV; however, PRSV-inoculated plants developed a systemic infection with accompanied symptoms and high levels of PRSV accumulation in noninoculated leaves. PI595203 was shown in previous studies to be resistant to PRSV. We show in this report that under greenhouse conditions and application of virus by mechanical inoculation, ‘AU-Performance’ was not resistant to infection by the three potyviruses.

scholarly journals Components of Arabidopsis Defense- and Ethylene-Signaling Pathways Regulate Susceptibility to Cauliflower mosaic virus by Restricting Long-Distance Movement

2007 ◽  
Vol 20 (6) ◽  
pp. 659-670 ◽  
Author(s):  
Andrew J. Love ◽  
Valérie Laval ◽  
Chiara Geri ◽  
Janet Laird ◽  
A. Deri Tomos ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Systemic Acquired Resistance ◽  
Fluorescent Protein ◽  
Acquired Resistance ◽  
Systemic Infection ◽  
Cauliflower Mosaic Virus ◽  
Virus Movement ◽  
Wild Type ◽  
Long Distance ◽  
Systemic Spread

We analyzed the susceptibility of Arabidopsis mutants with defects in salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET) signaling to infection by Cauliflower mosaic virus (CaMV). Mutants cpr1-1 and cpr5-2, in which SA-dependent defense signaling is activated constitutively, were substantially more resistant than the wild type to systemic infection, implicating SA signaling in defense against CaMV. However, SA-deficient NahG, sid2-2, eds5-1, and pad4-1 did not show enhanced susceptibility. A cpr5 eds5 double mutant also was resistant, suggesting that resistance in cpr5 may function partially independently of SA. Treatment of cpr5 and cpr5 eds5, but not cpr1, with salicyl-hydroxamic acid, an inhibitor of alternative oxidase, partially restored susceptibility to wild-type levels. Mutants etr1-1, etr1-3, and ein2-1, and two mutants with lesions in ET/JA-mediated defense, eds4 and eds8, also showed reduced virus susceptibility, demonstrating that ET-dependent responses also play a role in susceptibility. We used a green fluorescent protein (GFP)-expressing CaMV recombinant to monitor virus movement. In mutants with reduced susceptibility, cpr1-1, cpr5-2, and etr1-1, CaMV-GFP formed local lesions similar to the wild type, but systemic spread was almost completely absent in cpr1 and cpr5 and was substantially reduced in etr1-1. Thus, mutations with enhanced systemic acquired resistance or compromised ET signaling show diminished long-distance virus movement.

scholarly journals Temporal and Spatial Appearance of Recombinant Viruses Formed Between Cauliflower Mosaic Virus (CaMV) and CaMV Sequences Present in Transgenic Nicotiana bigelovii

1998 ◽  
Vol 11 (4) ◽  
pp. 309-316 ◽  
Author(s):  
Lorant Király ◽  
June E. Bourque ◽  
James E. Schoelz
Keyword(s):  
Transgenic Plants ◽  
Mosaic Virus ◽  
Leaf Tissue ◽  
Cauliflower Mosaic Virus ◽  
Recombinant Viruses ◽  
Predominant Type ◽  
Nicotiana Bigelovii ◽  
Temporal And Spatial ◽  
Systemic Symptoms ◽  
Symptom Type

Cauliflower mosaic virus (CaMV) strain CM1841 is able to recombine with a CaMV transgene sequence present in Nicotiana bigelovii. In the present study we have characterized the temporal and spatial appearance of recombinant viruses formed between CM1841 and the transgene within individual transgenic plants. CM1841 infections were initiated by mechanical inoculation and by agro-inoculation to nontransformed N. bigelovii and transgenic N. bigelovii that expressed the gene VI product of CaMV strain D4. In agroinoculated transgenic plants, inoculated leaf tissue turned necrotic around the point of agroinocu-lation, while chlorotic lesions appeared in the leaves inoculated with CM1841 virions. The first systemic symptoms in both agroinoculated and mechanically inoculated transgenic N. bigelovii consisted of necrotic patches. The predominant type of virus recovered from the inoculated and first systemically infected leaves was the wild-type CM1841 rather than a recombinant. As the infection progressed in the transgenic plants, symptoms changed from necrosis in the lower leaves to a chlorotic mosaic in the upper leaves. This shift in symptom type was associated with the recovery of recombinant viruses, indicating that the recombinants predominated only in later stages of pathogenesis.

scholarly journals Differential Induction of Symptoms in Arabidopsis by P6 of Cauliflower mosaic virus

2003 ◽  
Vol 16 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Weichang Yu ◽  
Jane Murfett ◽  
James E. Schoelz
Keyword(s):  
Transgenic Plants ◽  
Mosaic Virus ◽  
Systemic Infection ◽  
Cauliflower Mosaic Virus ◽  
Minor Role ◽  
Primary Role ◽  
Complementation Assay ◽  
Unusual Variant ◽  
A Minor

The gene VI protein (P6) of Cauliflower mosaic virus (CaMV) functions as a virulence factor in crucifers by eliciting chlorotic symptoms in infected plants. The ability to induce chlorosis has been associated previously with P6 through gene-swapping experiments between strains and through the development of transgenic plants that express P6. The primary role that has been identified for P6 in the CaMV infection cycle is to modify the host translation machinery to facilitate the translation of the polycistronic CaMV 35S RNA. This function for P6 has been designated as the translational transactivator (TAV) function. In the present study, we have characterized an unusual variant of P6, derived from CaMV strain D4, that does not induce chlorosis upon transformation into Arabidopsis thaliana. The level of D4 P6 produced in transgenic Arabidopsis line D4-2 was comparable to the amount found in transgenic plants homozygous for W260 and CM1841 P6, two versions of P6 that induce strong chlorotic symptoms and stunting in Arabidopsis. A complementation assay proved that P6 expressed in the D4-2 line was functional, as it could support the systemic infection of a CM1841 mutant that contained a lethal frame-shift mutation within gene VI. This complementation assay allowed us to separately assess the contribution of CM1841 gene VI to symptom development versus the contribution of other CM1841 genes. Furthermore, a previous study had shown that the TAV activity of D4 P6 was comparable to that of W260 P6. That comparative analysis of TAV function, coupled with the characterization of the D4-2 transgenic line in the present paper, indicates that the TAV function of P6 may play only a minor role in the development of chlorotic symptoms.

Structure of the Mature P3-virus Particle Complex of Cauliflower Mosaic Virus Revealed by Cryo-electron Microscopy

2005 ◽  
Vol 346 (1) ◽  
pp. 267-277 ◽  
Author(s):  
Célia Plisson ◽  
Marilyne Uzest ◽  
Martin Drucker ◽  
Rémy Froissart ◽  
Christian Dumas ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Mosaic Virus ◽  
Virus Particle ◽  
Cauliflower Mosaic Virus ◽  
Cryo Electron Microscopy

scholarly journals Selective autophagy limits cauliflower mosaic virus infection by NBR1-mediated targeting of viral capsid protein and particles

2017 ◽  
Vol 114 (10) ◽  
pp. E2026-E2035 ◽  
Author(s):  
Anders Hafrén ◽  
Jean-Luc Macia ◽  
Andrew J. Love ◽  
Joel J. Milner ◽  
Martin Drucker ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Virus Particle ◽  
Plant Immunity ◽  
Survival Function ◽  
Virus Production ◽  
Cauliflower Mosaic Virus ◽  
Capsid Proteins ◽  
Independent Manner ◽  
Particle Assembly ◽  
Selective Autophagy

Autophagy plays a paramount role in mammalian antiviral immunity including direct targeting of viruses and their individual components, and many viruses have evolved measures to antagonize or even exploit autophagy mechanisms for the benefit of infection. In plants, however, the functions of autophagy in host immunity and viral pathogenesis are poorly understood. In this study, we have identified both anti- and proviral roles of autophagy in the compatible interaction of cauliflower mosaic virus (CaMV), a double-stranded DNA pararetrovirus, with the model plantArabidopsis thaliana. We show that the autophagy cargo receptor NEIGHBOR OF BRCA1 (NBR1) targets nonassembled and virus particle-forming capsid proteins to mediate their autophagy-dependent degradation, thereby restricting the establishment of CaMV infection. Intriguingly, the CaMV-induced virus factory inclusions seem to protect against autophagic destruction by sequestering capsid proteins and coordinating particle assembly and storage. In addition, we found that virus-triggered autophagy prevents extensive senescence and tissue death of infected plants in a largely NBR1-independent manner. This survival function significantly extends the timespan of virus production, thereby increasing the chances for virus particle acquisition by aphid vectors and CaMV transmission. Together, our results provide evidence for the integration of selective autophagy into plant immunity against viruses and reveal potential viral strategies to evade and adapt autophagic processes for successful pathogenesis.

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