Lettuce necrotic yellows virus

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Structure of the C-Terminal Domain of Lettuce Necrotic Yellows Virus Phosphoprotein

Structure of the C-Terminal Domain of Lettuce Necrotic Yellows Virus Phosphoprotein

Lettuce necrotic yellows virus (LNYV) is a prototype of the plant-adapted cytorhabdoviruses. Through a meta-prediction of dis- order, we localized a folded C-terminal domain in the amino acid sequence of its phosphoprotein. This domain consists of an autonomous folding unit that is monomeric in solution. Its structure, solved by X-ray crystallography, reveals a lollipop-shaped structure comprising five helices. The structure is different from that of the corresponding domains of other Rhabdoviridae, Fi- loviridae, and Paramyxovirinae; only the overall topology of the polypeptide chain seems to be conserved, suggesting that this domain evolved under weak selective pressure and varied in size by the acquisition or loss of functional modules.
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Asynchronous Accumulation of Lettuce Infectious Yellows Virus RNAs 1 and 2 and Identification of an RNA 1 trans  Enhancer of RNA 2 Accumulation

Asynchronous Accumulation of Lettuce Infectious Yellows Virus RNAs 1 and 2 and Identification of an RNA 1 trans Enhancer of RNA 2 Accumulation

Replication enhancers have been reported for several mul- tipartite plant viruses and include the ␥RNA-encoded ␥B of Barley stripe mosaic virus (BSMV; 19), the Cowpea mosaic virus (CPMV) M-RNA-encoded 58-kDa protein (4), the Beet ne- crotic yellow vein virus (BNYVV)-encoded P14 (8), and the Peanut clump virus (PCV) RNA 1-encoded P15 (9). The BSMV ␥B, the BNYVV P14, and the PCV P15 proteins all belong to a group of cysteine-rich proteins, and P14 shares weak but statistically significant similarity with other nucleic acid binding proteins (8). These cysteine-rich proteins influ- ence or enhance replication for all genomic components of their respective virus. In contrast, the CPMV 58-kDa protein is a template-selective replication enhancer. The CPMV 58-kDa protein is needed for efficient replication of the CPMV M- RNA but not the CPMV B-RNA; thus, it is a cis replication enhancer. Interestingly, a RNA sequence located within Red clover necrotic mosaic virus (RCNMV) genomic RNA 2 has recently been identified as a transcriptional enhancer, func- tioning in trans for the synthesis of an RCNMV RNA 1 sub- genomic RNA (22).
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Two Crinivirus-Conserved Small Proteins, P5 and P9, Are Indispensable for Efficient Lettuce infectious yellows virus Infectivity in Plants.

Two Crinivirus-Conserved Small Proteins, P5 and P9, Are Indispensable for Efficient Lettuce infectious yellows virus Infectivity in Plants.

Keywords: Lettuce infectious yellows virus ; P5; P9; small ORFs; virus infectivity; ER stress 1. Introduction RNA viruses have evolved to compress maximal coding and regulatory information into minimal sequence space. Small open reading frames (ORFs) that encode peptides of less than 100 amino acids, a strategy often employed by viruses to minimize the size of their genome, still perform essential roles in virus infection [ 1 ]. For example, the 6-kDa viral protein 6K2 of Turnip mosaic virus (TuMV, Potyvirus) is a membrane-associated protein that induces the formation of endoplasmic reticulum (ER)-derived vesicles for viral genome amplification, and mediates their export from the ER for virus systemic infection [ 2 , 3 ]. Another 6-kDa potyviral protein, 6K1, is also required for viral replication and targets the viral replication complex at the early stage of infection [ 4 ]. In another example, two consecutive small proteins of 7-kDa (P7A and P7B) encoded by Melon necrotic spot virus (MNSV) are involved in virus cell-to-cell movement, and P7B has shown to be a type II integral membrane protein that is essential for ER export, transport to the Golgi apparatus and finally to the plasmadesmata (PD) [ 5 – 7 ]. However, for many viruses, the very small ORFs/proteins are often overlooked due to their short sequences and uncertain significance. It is imperative to identify the coding regions and understand their functions to decipher how these small ORFs/proteins promote the infection cycle.
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Effects of Point Mutations in the Readthrough Domain of the Beet Western Yellows Virus Minor Capsid Protein on Virus Accumulation In Planta and on Transmission by Aphids

Effects of Point Mutations in the Readthrough Domain of the Beet Western Yellows Virus Minor Capsid Protein on Virus Accumulation In Planta and on Transmission by Aphids

Point mutations were introduced into or near five conserved sequence motifs of the readthrough domain of the beet western yellows virus minor capsid protein P74. The mutant virus was tested for its ability to accu- mulate efficiently in agroinfected plants and to be transmitted by its aphid vector, Myzus persicae. The stability of the mutants in the agroinfected and aphid-infected plants was followed by sequence analysis of the progeny virus. Only the mutation Y201D was found to strongly inhibit virus accumulation in planta following agroin- fection, but high accumulation levels were restored by reversion or pseudoreversion at this site. Four of the five mutants were poorly aphid transmissible, but in three cases successful transmission was restored by pseudo- reversion or second-site mutations. The same second-site mutations in the nonconserved motif PVT(32-34) were shown to compensate for two distinct primary mutations (R24A and E59A/D60A), one on each side of the PVT sequence. In the latter case, a second-site mutation in the PVT motif restored the ability of the virus to move from the hemocoel through the accessory salivary gland following microinjection of mutant virus into the aphid hemocoel but did not permit virus movement across the epithelium separating the intestine from the hemocoel. Successful movement of the mutant virus across both barriers was accompanied by conversion of A59 to E or T, indicating that distinct features of the readthrough domain in this region operate at different stages of the transmission process.
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Adaptive Covariation between the Coat and Movement Proteins of Prunus Necrotic Ringspot Virus

Adaptive Covariation between the Coat and Movement Proteins of Prunus Necrotic Ringspot Virus

The relative functional and/or structural importance of different amino acid sites in a protein can be assessed by evaluating the selective constraints to which they have been subjected during the course of evolution. Here we explore such constraints at the linear and three-dimensional levels for the movement protein (MP) and coat protein (CP) encoded by RNA 3 of prunus necrotic ringspot ilarvirus (PNRSV). By a maximum-parsimony approach, the nucleotide sequences from 46 isolates of PNRSV varying in symptomatol- ogy, host tree, and geographic origin have been analyzed and sites under different selective pressures have been identified in both proteins. We have also performed covariation analyses to explore whether changes in certain amino acid sites condition subsequent variation in other sites of the same protein or the other protein. These covariation analyses shed light on which particular amino acids should be involved in the physical and functional interaction between MP and CP. Finally, we discuss these findings in the light of what is already known about the implication of certain sites and domains in structure and protein-protein and RNA-protein interactions.
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Interaction between Long-Distance Transport Factor and Hsp70-Related Movement Protein of Beet Yellows Virus

Interaction between Long-Distance Transport Factor and Hsp70-Related Movement Protein of Beet Yellows Virus

Moreover, coexpression of Hsp70h, N42, or C23 with p20-GFP results in relocalization of the latter product, suggesting that p20 can interact with Hsp70h or its domains in live plant cells. p20 is a long-distance transport factor. What is the primary function of p20 in the BYV life cycle? Previous work demon- strated that p20 is dispensable for BYV replication (39) and is not essential for virus cell-to-cell movement, although it might have an accessory role in the latter process (2). The interaction of p20 with Hsp70h, which is one of the three BYV MPs (40), prompted us to revisit the role of p20 in cell-to-cell movement. A previously characterized p20 mutant, ⌬p20, was poten- tially capable of expressing C-terminal fragments of p20 (Fig. 5). It could not be excluded that this fragment was partially functional in the cell-to-cell movement of the corresponding mutant variant (2). Deletion of the RNA region encoding this fragment was impractical because it would inactivate a sub- genomic promoter that governs expression of a replication- associated BYV protein, p21 (39). Consequently, we designed two additional point mutations by introducing premature stop codons in place of the 49th and 81st p20 codons. These mu- tants could direct the translation of only short, N-terminal p20 peptides (Fig. 5). Each mutation was introduced into GFP- tagged BYV, and the resulting mutant BYV-GFP variants were inoculated into the local lesion host plants (40). Exami- nation of these mutants demonstrated that each of them was capable of cell-to-cell movement. The Stop-49 and Stop-81 mutants produced multicellular infection foci with mean diam- eters of 4.0 ⫾ 2.3 and 2.1 ⫾ 1.1 cells, respectively. The infec- tion foci formed by the parental BYV-GFP variant had mean diameters of 5.1 ⫾ 2.8 cells. These data confirmed our previous conclusion that p20 is not essential for the BYV cell-to-cell movement, although its inactivation results in a less efficient local spread.
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The determination of the spatial and temporal distribution of Aster Yellows phytoplasma in grapevine

The determination of the spatial and temporal distribution of Aster Yellows phytoplasma in grapevine

Phytoplasmas are obligate bacterial parasites, which only replicate and survive intra- cellularily within insect or plant hosts. They are known to cause several diseases in grapevine namely; Bois Noir (BN), Flavescence dorée (FD), Australian grapevine yellows and the focus of this study, Aster Yellows (AY). Internationally, these diseases have caused between 20 – 30% and sometimes as high as 80% loss of yield in vines (Magarey, 1986). Grapevine Yellows (GY), the name given to the group of diseases caused by these pathogens, is known to have detrimental effects in vineyards across the world. The pathogen has induced severe economic losses in the production of wine in Europe and Australia (Lee et al, 2000). Since methods of disease control have been implemented, this yield loss has decreased significantly, demonstrating the necessity of research into controlling the pathogen. Recently, Aster Yellows phytoplasma was discovered in the Vredendal and the Wabooms River wine producing areas in South Africa (Engelbrecht et al, 2010) which could be pernicious to the country’s wine industry. It is thus crucial that different methods of control as well as accurate diagnosis be investigated with the aim of understanding more about phytoplasmas and reducing their ramifications.
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Prevalence of aster yellows (AY) and elm yellows (EY) group phytoplasmas in symptomatic grapevines in three areas of northern Italy

Prevalence of aster yellows (AY) and elm yellows (EY) group phytoplasmas in symptomatic grapevines in three areas of northern Italy

While no evidence was obtained for infection of grapevines by strains related to X-disease phytoplasmas (group 16Sriii), phytoplasmas related to elm yellows (group 16SrV),[r]

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Cabbage yellows, caused by Fusarium Conglutinans, in Iowa

Cabbage yellows, caused by Fusarium Conglutinans, in Iowa

The most noticeable and characteristic appearance of yellows on seedlings is a: bright yellowing, turning to gray as the leaf wilts. I f the plants in the infested seedbed are kept cool and moist and are in good, rich soil, the disease may not show up to any great degree. This may lead the grower to think his plants are healthy and he may unwittingly spread infection to new fields by means of these plants. It is probable that the majority of fields are originally infested from such transplants. Very young seedlings are not attacked by the yellows organism. There follows a period of 12 to 14 days, often longer, after the seedling comes up when no sign of yellows can be found. To all appear­ ances the plants are healthy. A t this time the plants are estab­ lishing their root systems while depending partly on the food from the seeds. Apparently this length" of time is required for the fungus to gain entrance into the root hairs and establish it­ self in the vascular system of the plant. A t this time, if con­ ditions are favorable for the causal agent, the symptoms of yel­ lows begin to appear.
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Simultaneous detection and differentiation of three genotypes of Brassica yellows virus by multiplex reverse transcription polymerase chain reaction

Simultaneous detection and differentiation of three genotypes of Brassica yellows virus by multiplex reverse transcription polymerase chain reaction

N. benthamiana leaf tissues infected with BrYV-A, -B, C were used to standardize the multiplex RT-PCR. Each of these three genotypes infecting N. benthamiana was identified by RT-PCR and sequencing. Plasmids contain- ing full-length genomic sequences of BrYV-A (Accession No. NC016038), BrYV-B (Accession No.HQ388351), BrYV-C (Accession No. KF015269), Turnip mosaic virus(TuMV) (Accession No. AF169561.2), Cucumber mo- saic virus (CMV Fny strain) (Accession No. NC002034, NC002035, NC001440), Cucurbit aphid-borne yellows virus (CABYV) (Accession No. HQ439023), Beet western yellows virus Inner Mongolia isolate (BWYV-IM) (Acces- sion No. EU636991), and plasmids containing partial gen- omic sequences of TuYV were used to test specificity of the multiplex PCR in this study. The plasmid pMD19- TuYV-P0 contained the complete sequence of the ORF0 of TuYV (Accession No. NC003743) and the plasmid pMD19-56#-1 contained the 4959–5163 nt sequence of TuYV which shared 96.4% nucleotide sequence identity with TuYV isolate Anhui (Accession No. KR706247.1).
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Identification and QTL mapping of resistance to Turnip yellows virus (TuYV) in oilseed rape, Brassica napus

Identification and QTL mapping of resistance to Turnip yellows virus (TuYV) in oilseed rape, Brassica napus

ing experiments showed a clear bimodal distribution of susceptible to resistant plants, as would be predicted for a 1:1 segregation of a strong monogenic trait. Thus, TuYV resistance in Yudal may depend on additional contributing genes, environmental factors and/or may be an artefact of the phenotyping of this partially dominant trait. The mapping of TuYV resistance in ‘R54’ showed a clear single QTL, but was based on phenotypes also not showing a bimodal distribution (Dreyer et al. 2001). Nevertheless, the markers derived from this mapping approach have been very success- ful in introgressing the resistance from ‘R54’ into the com- mercial oilseed rape variety ‘Caletta’ (Graichen and Peterka 1999). A second QTL qTUYVC5 was identified in one of the DH experiments (SP2), explaining 11.9% of the pheno- typic variation, acting additively, without interaction with qTUYVA4. The estimated effects of the QTLs on Chr A04 and Chr C05 (Table 2) showed opposite effects of allelic substitution, suggesting that both parental lines contributed to the resistance response. Although susceptible to TuYV, Darmor-bzh did not show the highest virus titre amongst the 27 tested B. napus accessions. However, as the qTUYVC5 effect was only seen in one of the two experiments on the DYDH lines, it remains speculative as to whether the slightly lower TuYV infection in Darmor-bzh was actually caused by genetic factors. No additional significant QTL were detected in either the DYDH experiment SP1 or in the segregating BC 1 population, suggesting that the contribution
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Changes in Bemisia tabaci feeding behaviors caused directly and indirectly by cucurbit chlorotic yellows virus

Changes in Bemisia tabaci feeding behaviors caused directly and indirectly by cucurbit chlorotic yellows virus

Bemisia tabaci (Gennadius) (Hemiptera: Aleyrodidae) is considered as a cryptic species with at least 39 mor- phologically indistinguishable biotypes, which are often reproductively isolated [19–21]. Biotype B (also referred to as Middle East-Asia Minor 1) and biotype Q (also re- ferred to as Mediterranean) are the two most invasive and destructive in B. tabaci [19]. In the past 30 years, B. tabaci biotypes B and Q have invaded many countries worldwide and displaced some indigenous cryptic bio- types [19]. Both biotypes B and Q can seriously damage plants by feeding upon phloem sap and secreting honey- dew, which can result in fungal growth on damaged plant tissues. In addition, B. tabaci can transmit plant vi- ruses, some of which could be devastating to crop plants [22, 23]. To date, more than 200 plant virus species have been reported to be transmitted by B. tabaci [24–26]. Viruses in the genera of Begomovirus, Crinivirus, Ipomo- virus, Carlavirus and Torradovirus can be transmitted by B. tabaci. Viral epidemic outbreak of whitefly-transmitted viruses in various regions is often a result of high population densities, especially high abundance of bio- types B and Q [22, 27, 28].
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Identification and QTL mapping of resistance to Turnip yellows virus (TuYV) in oilseed rape, Brassica napus

Identification and QTL mapping of resistance to Turnip yellows virus (TuYV) in oilseed rape, Brassica napus

distribution of susceptible to resistant plants, as would be predicted for a 1:1 segregation of a strong monogenic trait. Thus, TuYV resistance in Yudal may depend on additional contributing genes, environmental factors and/or may be an artefact of the phenotyping of this partially dominant trait. The mapping of TuYV resistance in ‘R54’, showed a clear single QTL, but was based on phenotypes also not showing a bimodal distribution (Dreyer et al. 2001). Nevertheless, the markers derived from this mapping approach have been very successful in introgressing the resistance from ‘R54’ in to the commercial oilseed rape variety ‘Caletta’ (Graichen and Peterka 1999). A second QTL qTUYVC5 was identified in one of the DH experiments (SP2), explaining 11.9% of the phenotypic variation, acting additively, without interaction with qTUYVA4. The estimated effects of the QTLs on Chr A04 and Chr C05 (Table 2) showed opposite effects of allelic substitution, suggesting that both parental lines contributed to the resistance response. Although susceptible to TuVV, Darmor-bzh did not show the highest virus titre amongst the 27 tested B. napus accessions. However, as the qTUYVC5 effect was only seen in one of the two experiments on the DYDH lines, it remains speculative as to whether the slightly lower TuYV infection in Darmor-bzh was actually caused by genetic factors. No additional significant QTL were detected in either the DYDH experiment SP1, nor in the segregating BC 1 population, suggesting, that the contribution of qTUYVC5
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The 64-Kilodalton Capsid Protein Homolog of Beet Yellows Virus Is Required for Assembly of Virion Tails

The 64-Kilodalton Capsid Protein Homolog of Beet Yellows Virus Is Required for Assembly of Virion Tails

How could this unique constellation of genes with dual func- tions in virion formation and cell-to-cell movement evolve? This work and previous analyses (7) showed that one of the underlying mechanisms was tandem gene duplication, which occurred at least twice to yield the coding regions for CPm and the CP-like domain of p64 (Fig. 2). Since the three CP-like domain-containing genes are present in all of the closterovi- ruses whose genomes have been sequenced so far, it appears that both duplications occurred prior to the divergence of these viruses from their common ancestor. Other important events in the evolution of closteroviruses apparently included acquisition of the coding regions for Hsp70h and the N-termi- nal domain of p64. In the former case, it appears obvious that an ancestral closterovirus captured a cellular mRNA for Hsp70 (1) whereas the origin of the upstream portion of the p64 gene remains obscure. In addition to being an MP and an essential virion component (5, 36), Hsp70h provides a docking site for long-distance transport factor p20, which is required for sys- temic virus spread through the plant vasculature (38). Al- though p20 is associated with virions, unlike other virion pro- teins, it is not essential for assembly or cell-to-cell movement. The evolutionary scenario for tailed closterovirus virions can be interpreted as a hierarchical buildup of virion functions from merely protecting the genome to driving cell-to-cell movement to mediating long-distance transport of the virus. It seems likely that, during closterovirus evolution, the selective advantage conferred on the virus by these increasingly complex devices for virus-host interaction was a driving force behind the evolution of the mechanisms of subgenomic RNA synthesis and its regulation and, accordingly, the overall increase in genome size.
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Effects of Point Mutations in the Major Capsid Protein of Beet Western Yellows Virus on Capsid Formation, Virus Accumulation, and Aphid Transmission

Effects of Point Mutations in the Major Capsid Protein of Beet Western Yellows Virus on Capsid Formation, Virus Accumulation, and Aphid Transmission

Point mutations were introduced into the major capsid protein (P3) of cloned infectious cDNA of the polerovirus beet western yellows virus (BWYV) by manipulation of cloned infectious cDNA. Seven mutations targeted sites on the S domain predicted to lie on the capsid surface. An eighth mutation eliminated two arginine residues in the R domain, which is thought to extend into the capsid interior. The effects of the mutations on virus capsid formation, virus accumulation in protoplasts and plants, and aphid transmission were tested. All of the mutants replicated in protoplasts. The S-domain mutant W166R failed to protect viral RNA from RNase attack, suggesting that this particular mutation interfered with stable capsid formation. The R-domain mutant R7A/R8A protected ⬃ 90% of the viral RNA strand from RNase, suggesting that lower positive-charge density in the mutant capsid interior interfered with stable packaging of the complete strand into virions. Neither of these mutants systemically infected plants. The six remaining mutants properly packaged viral RNA and could invade Nicotiana clevelandii systemically following agroinfection. Mutant Q121E/ N122D was poorly transmitted by aphids, implicating one or both targeted residues in virus-vector interac- tions. Successful transmission of mutant D172N was accompanied either by reversion to the wild type or by appearance of a second-site mutation, N137D. This finding indicates that D172 is also important for trans- mission but that the D172N transmission defect can be compensated for by a “reverse” substitution at another site. The results have been used to evaluate possible structural models for the BWYV capsid.
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Bark necrotic disease in a beech thicket

Bark necrotic disease in a beech thicket

Our results show that the necrotic disease on the stem and branch bark is quite common in young beech stands and has its dynamics and progression order. The analysis of the problem highlights the complexity of mutual relations between the growth of individual young beech trees and the necrotic disease on the bark of their stems and branches in the complex of a number of integrating factors and processes. It is necessary to emphasise the important fact of the re- generative capacity of beech individuals in relation to necrotic disease. Annually, on average 21.2% of stem wounds and 16.0% of branch wounds were healed, this is by 10.8 and 0.6% more than the occurrence of new stem and branch necroses during the same period, respectively. This means that under normal condi- tions (optimal growth conditions), the regeneration processes in a young beech stand are so intense that a significant recovery from necroses can gradually take place. This is also true of branches because in thick young beech stands, shaded and infected branches gradually die and fall off due to the competition. By finding that the occurrence and healing of the
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Molecular Basis for Mitochondrial Localization of Viral Particles during Beet Necrotic Yellow Vein Virus Infection

Molecular Basis for Mitochondrial Localization of Viral Particles during Beet Necrotic Yellow Vein Virus Infection

An intriguing aspect of the anchoring of P75 to the mito- chondrial membrane is the apparent flexibility in the recruit- ment of the hydrophobic domains ensuring membrane integra- tion. From computer analysis and from the literature (1), TM1 (amino acids 273 to 303 of P75) is the major hydrophobic domain in the N-terminal part of the RTD. Gain-of-function experiments with GFP fusions showed that TM1 is able to cooperate with the MTS to support anchoring of a reporter protein to the mitochondrial membrane. However, the dele- tion of TM1 from the otherwise complete P75 does not seem to greatly alter anchoring of the viral protein to the outer membranes of isolated mitochondria. It thus appears that dif- ferent hydrophobic domains can promote membrane anchor- ing after recognition of the mitochondria by the MTS. Indeed, the two other hydrophobic domains in the proximal part of the RTD, i.e., TM3 (amino acids 308 to 326 of P75) and TM4 (amino acids 373 to 394), are also able to support the MTS- mediated mitochondrial targeting in vivo. From the collected data, it seems plausible that the TM3-TM4 domain actually provides the final membrane-embedded anchor in the com- plete P75 context. Previous studies have shown that the Car- nation Italian ringspot virus replicase contains redundant infor- mation for mitochondrial targeting (55), so it cannot be excluded that BNYVV P75 similarly possesses redundant in- formation for membrane insertion. However, it seems likely
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Controlling downy mildew of lettuce

Controlling downy mildew of lettuce

Transplanting Bordeaux-treated Lettuce Seedlings. It has been observed by some commercial growers that when lettuce plants are sprayed with bordeaux shortly after transplanting, they show an unusual amount of wilting. Duggar’s investiga­ tions have a bearing on this point.* He shows that with potato foliage for a period of two to three hours following the appli­ cation of bordeaux mixture, the rate of loss of water by transpir­ ation was doubled. It appears, therefore, inadvisable to spray seedlings with bordeaux either immediately before or after transplanting. It has been the observation of the writer, how­ ever, that if bordeaux treatment is delayed until a day or two after transplanting, no apparent wilting follows.
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Grapevine yellows affecting the Croatian indigenous grapevine cultivar Grk

Grapevine yellows affecting the Croatian indigenous grapevine cultivar Grk

Abstract – The grapevine cultivar Grk, a close relative of Crljenak ka{telanski/Zinfandel, is grown exclusively in southern Croatia. Grapevine yellows-like symptoms were ob- served on vines in the vineyards in Lumbarda (southern Croatia) and in propagated grape- vines near Zadar and Zagreb. The majority of the detected phytoplasma isolates belonged to the 16SrI group. However, RFLP pattern and R16F2n/R2 fragment sequence assigned one isolate to the 16SrIII group. Thus far, on cv. Grk, phytoplasmas belonging to three dif- ferent groups have been detected: 16SrI, 16SrIII, and 16SrXII, which was confirmed previ- ously. Aside from the 16SrI, 16SrV and 16SrXII phytoplasma groups previously found on grapevines in Croatia, the finding of 16SrIII group, which is not common on grapevines in Europe, adds to the diversity of phytoplasmas in a very small geographic region. Key words: molecular detection, phytoplasma, RFLP, Vitis vinifera cv. Grk
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Influence of harvest timing, fungicides, and Beet Necrotic Yellow Vein Virus on sugar beet storage

Influence of harvest timing, fungicides, and Beet Necrotic Yellow Vein Virus on sugar beet storage

In areas with cold winter temperatures such as North Dakota, roots in both outdoor and indoor piles usually are frozen solid by mid- December when ambient temperatures average #− 10°C, which sta- bilizes the roots for long-term storage (6,8,9). In areas such as Idaho, Wyoming, and Michigan, with roots stored under ambient condi- tions, only roots near the pile surface freeze because temperatures are either not cold enough or fluctuate too much to maintain the roots in the whole pile in a frozen state (8,9). Roots stored under such am- bient conditions are subject to freeze-thaw cycles, wet weather, warm nights which does not allow for cooling of the piles of roots, and control of microbial growth (8,9,51,52,62). For example, when 20% of the sugar beet root surface was covered by fungal growth, the respiration rate of the stored sugar beet roots doubled within 1 month (32). In addition, roots from plants subjected to diseases in the field such as Aphanomyces root rot (Aphanomyces cochlioides Drechsler), Cercospora leaf spot (Cercospora beticola Sacc.), curly top (Beet curly top virus), Fusarium yellows (Fusarium oxysporum f. sp. betae W. C. Snyder & H. N. Hansen), Rhizoctonia root rot (Rhizoctonia solani K¨uhn), and rhizoma- nia (Beet necrotic yellow vein virus [BNYVV]) store more poorly than roots produced by healthy plants (15–17,27,44,50–52).
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