scholarly journals Localization of genetic determinants for pathogenicity of Maize dwarf mosaic virus and Bermudagrass southern mosaic virus

2019 ◽  
Author(s):  
Farveh sadat Mostafavi Neyshabouri ◽  
Ahad Yamchi ◽  
Seyed Kazem Sabbagh ◽  
Mahmoud Masumi
Keyword(s):  
Coat Protein ◽  
Mosaic Virus ◽  
Genomic Sequence ◽  
Biological Properties ◽  
Maize Dwarf Mosaic Virus ◽  
Wild Type ◽  
Genetic Determinants ◽  
Rhopalosiphum Maidis ◽  
Qrt Pcr ◽  
Nucleotide Region

AbstractMaize dwarf mosaic virus (MDMV) and Bermuda grass southern mosaic virus (BgSMV) are economically important potyviruses of cereals. BgSMV is very similar in genomic sequence to MDMV, but cannot infect Johnsongrass and is not transmitted by Rhopalosiphum maidis. Comparison of their genomes showed an additional stretch of 90 nucleotides in BgSMV coat protein but not in MDMV. Since the 90-nucleotide region is located in the N-terminal of BgSMV coat protein, it seems to have a role in biological properties such as vector transmission and pathogenicity. Recombinant virus constructs were made with and without the 90 nucleotides using SOEing PCR (MDMV (+90) and BgSMV (−90). Johnsongrass plants inoculated with the wild-type MDMV and recombinant BgSMV (−90) showed mosaic symptoms after 16 and 23 days, respectively, whereas plants inoculated with the wild-type BgSMV and recombinant MDMV (+90) didn’t show any symptoms until three months after inoculation. The qRT-PCR results detected significantly higher levels of BgSMV (−90) and MDMV compared to BgSMV and MDMV (+90), respectively. Also, R. maidis was able to transfer only the wild type MDMV and BgSMV (−90) from infected to healthy plants. These results confirmed that the insertion of the 90-nt region into the coat protein of MDMV affects the pathogenicity of the virus.

The genomic sequence and biological properties of Pennisetum mosaic virus, a novel monocot-infecting potyvirus

2008 ◽  
Vol 153 (5) ◽  
pp. 921-927 ◽  
Author(s):  
C. L. Deng ◽  
W. J. Wang ◽  
Z. Y. Wang ◽  
X. Jiang ◽  
Y. Y. Cao ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Genomic Sequence ◽  
Biological Properties

scholarly journals CRISPR/Cas9-mediated resistance to cauliflower mosaic virus

2017 ◽  
Author(s):  
Haijie Liu ◽  
Cara L. Soyars ◽  
Jianhui Li ◽  
Qili Fei ◽  
Guijuan He ◽  
...  
Keyword(s):  
Coat Protein ◽  
Transgenic Plants ◽  
Mosaic Virus ◽  
Crop Production ◽  
Cauliflower Mosaic Virus ◽  
Coat Proteins ◽  
Small Interfering Rnas ◽  
Wild Type ◽  
Dna Breaks ◽  
Virus Control

SummaryViral diseases are a leading cause of worldwide yield losses in crop production. Breeding of resistance genes (R gene) into elite crop cultivars has been the standard and most cost-effective practice. However, R gene-mediated resistance is limited by the available R genes within genetic resources and in many cases, by strain specificity. Therefore, it is important to generate new and broad-spectrum antiviral strategies. The CRISPR-Cas9 (clustered regularly interspaced palindromic repeat, CRISPR-associated) editing system has been employed to confer resistance to human viruses and several plant single-stranded DNA geminiviruses, pointing out the possible application of the CRISPR-Cas9 system for virus control. Here we demonstrate that strong viral resistance to cauliflower mosaic virus (CaMV), a pararetrovirus with a double-stranded DNA genome, can be achieved through Cas9-mediated multiplex targeting of the viral coat protein sequence. We further show that small interfering RNAs (siRNA) are produced and mostly map to the 3' end of guide RNAs (gRNA), although very low levels of siRNAs map to the spacer region as well. However, these siRNAs are not responsible for the inhibited CaMV infection because there is no resistance if Cas9 is not present. We have also observed edited viruses in systematically infected leaves in some transgenic plants, with short deletions or insertions consistent with Cas9-induced DNA breaks at the gRNA target sites in coat protein coding sequence. These edited coat proteins, in most cases, led to earlier translation stop and thus, non-functional coat proteins. We also recovered wild-type CP sequence in these infected transgenic plants, suggesting these edited viral genomes were packaged by wild-type coat proteins. Our data demonstrate that the CRISPR-Cas9 system can be used for virus control against plant pararetroviruses with further modifications.

scholarly journals In Vivo Packaging of Brome Mosaic Virus RNA3, but Not RNAs 1 and 2, Is Dependent on a cis-Acting 3′ tRNA-Like Structure

2006 ◽  
Vol 81 (1) ◽  
pp. 173-181 ◽  
Author(s):  
Padmanaban Annamalai ◽  
A. L. N. Rao
Keyword(s):  
Coat Protein ◽  
Mosaic Virus ◽  
Nicotiana Benthamiana ◽  
Untranslated Region ◽  
Northern Blot Analysis ◽  
Brome Mosaic Virus ◽  
Wild Type ◽  
Cis Acting

ABSTRACT The four encapsidated RNAs of brome mosaic virus (BMV; B1, B2, B3, and B4) contain a highly conserved 3′ 200-nucleotide (nt) region encompassing the tRNA-like structure (TLS) which is required for packaging in vitro (Y. G. Choi, T. W. Dreher, and A. L. N. Rao, Proc. Natl. Acad. Sci. USA 99:655-660, 2002). To validate these observations in vivo, we performed packaging assays using Agrobacterium-mediated transient expression of RNAs and coat protein (CP) (P. Annamalai and A. L. N. Rao, Virology 338:96-111, 2005). Coexpression of TLS-less constructs of B1 or B2 or B3 and CP mRNAs in Nicotiana benthamiana leaves resulted in packaging of TLS-less B1 and B2 but not B3, suggesting that packaging of B3 requires the TLS in cis. This conjecture was confirmed by the efficient packaging of a B3 chimera in which the viral TLS was replaced with a cellular tRNATyr. When N. benthamiana leaves were infiltrated with a mixture of transformants containing wild-type B1 (wtB1) plus wtB2 plus a TLS-less B3 (wtB1+wtB2+TLS-lessB3), the 3′ end of progeny B3 was restored by heterologous recombination with that of either B1 or B2. This intrinsic cis-requirement of TLS in promoting B3 packaging was further confirmed when a mixture containing agrotransformants of TLS-less B1+B2+B3 was supplemented with either wtB4 or a 3′ 200-nt or 3′ 336-nt untranslated region (UTR) of B3. Northern blot analysis followed by sequencing of B3 progeny revealed that replication of TLS-less B3, but not TLS-less B1 or B2, was fully restored due to recombination with TLS from transiently expressed wtB4 or the B3 3′ UTR. Collectively, these observations suggested that the requirement of a cis-acting TLS is distinct for B3 compared with B1 or B2.

scholarly journals Complete Genome Characterization and Coat Protein Genealogy of Isolates of Maize dwarf mosaic virus from Johnsongrass and Maize in Oklahoma and Missouri

Plant Disease ◽  
2020 ◽  
Vol 104 (4) ◽  
pp. 1214-1223
Author(s):  
Dulanjani Wijayasekara ◽  
Akhtar Ali
Keyword(s):  
Coat Protein ◽  
Mosaic Virus ◽  
Complete Genome ◽  
Purifying Selection ◽  
Aphid Transmission ◽  
The United States ◽  
Mosaic Disease ◽  
Maize Dwarf Mosaic Virus ◽  
Maize Cultivars ◽  
Nucleotide Insertion

Maize dwarf mosaic virus (MDMV) significantly affects maize production worldwide, including the United States. This study describes the distribution and biological and molecular characterization of MDMV isolates from Johnsongrass and maize. A total of 262 samples (symptomatic = 214, asymptomatic = 48) were collected in Oklahoma and Missouri during 2016, 2017, and 2019 growing seasons. Based on a dot-immunobinding assay (DIBA), the average incidence of maize dwarf mosaic disease varied from ∼71% (79/111) in 2016, ∼76% (81/106) in 2017, and 62% (28/45) in 2019. Sixty-five DIBA-positive samples for MDMV were further confirmed by RT-PCR, and the complete coat protein (CP) gene was cloned and sequenced. Phylogenetic analysis of 132 isolates (This study = 65; GenBank = 67) revealed two main groups (G1 and G2) of MDMV isolates. All 65 MDMV isolates contained a 39-nucleotide insertion in the N-terminal region of CP genes and clustered in G1 which were different from the isolates in G2, without 39-nucleotide insertion. The first complete genome (9,563 nucleotides) of a MDMV isolate (Bixby1) from Johnsongrass was sequenced, which was distantly related to eight previously reported MDMV isolates from maize. The dN/dS ratio showed mostly purifying selection on each of cistrons except 6K1 being subjected to the diversifying selection. Further analyses revealed three putative recombination events between MDMV-Bixby1 and MDMV isolates from other countries. The successful mechanical and aphid transmission of MDMV-Bixby1 onto maize cultivars was achieved. Altogether, this information showed that Johnsongrass harbors genetically diverse MDMV isolates, which could pose a threat to cultivated crops such as maize and sorghum.

scholarly journals Wheat streak mosaic virus Coat Protein Deletion Mutants Elicit More Severe Symptoms Than Wild-Type Virus in Multiple Cereal Hosts

2017 ◽  
Vol 30 (12) ◽  
pp. 974-983 ◽  
Author(s):  
Satyanarayana Tatineni ◽  
Christian Elowsky ◽  
Robert A. Graybosch
Keyword(s):  
Amino Acids ◽  
Coat Protein ◽  
Mosaic Virus ◽  
Wheat Streak Mosaic Virus ◽  
Wild Type Virus ◽  
Deletion Mutants ◽  
Major Protein ◽  
Type Virus ◽  
Wild Type ◽  
Genomic Rnas

Previously, we reported that coat protein (CP) of Wheat streak mosaic virus (WSMV) (genus Tritimovirus, family Potyviridae) tolerates deletion of amino acids 36 to 84 for efficient systemic infection of wheat. In this study, we demonstrated that WSMV mutants with deletion of CP amino acids 58 to 84 but not of 36 to 57 induced severe chlorotic streaks and spots, followed by acute chlorosis in wheat, maize, barley, and rye compared with mild to moderate chlorotic streaks and mosaic symptoms by wild-type virus. Deletion of CP amino acids 58 to 84 from the WSMV genome accelerated cell-to-cell movement, with increased accumulation of genomic RNAs and CP, compared with the wild-type virus. Microscopic examination of wheat tissues infected by green fluorescent protein–tagged mutants revealed that infection by mutants lacking CP amino acids 58 to 84 caused degradation of chloroplasts, resulting in acute macroscopic chlorosis. The profile of CP-specific proteins was altered in wheat infected by mutants causing acute chlorosis, compared with mutants eliciting wild-type symptoms. All deletion mutants accumulated CP-specific major protein similarly to that in wild-type virus; however, mutants that elicit acute chlorosis failed to accumulate a 31-kDa minor protein compared with wild-type virus or mutants lacking amino acids 36 to 57. Taken together, these data suggest that deletion of CP amino acids 58 to 84 from the WSMV genome enhanced accumulation of CP and genomic RNA, altered CP-specific protein profiles, and caused severe symptom phenotypes in multiple cereal hosts.

Plants Transformed with a Mutant Alfalfa Mosaic Virus Coat Protein Gene Are Resistant to the Mutant but Not to Wild-Type Virus

Virology ◽  
1994 ◽  
Vol 203 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Peter E.M. Taschner ◽  
Guido Van Marle ◽  
Frans Th. Brederode ◽  
Nilgun E. Tumer ◽  
John F. Bol
Keyword(s):  
Coat Protein ◽  
Mosaic Virus ◽  
Coat Protein Gene ◽  
Protein Gene ◽  
Alfalfa Mosaic Virus ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Virus Coat Protein ◽  
Virus Coat
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