Recombination of strain O segments to HCpro‐encoding sequence of strain N of Potato virus Y modulates necrosis induced in tobacco and in potatoes carrying resistance genes Ny or Nc

Hypersensitive resistance (HR) to strains O and C of Potato virus Y (PVY, genus Potyvirus) is conferred by potato genes Ny_tbr and Nc_tbr, respectively; however, PVY N strains overcome these resistance genes. The viral helper component proteinases (HCpro, 456 amino acids) from PVY^N and PVY^O are distinguished by an eight‐amino‐acid signature sequence, causing HCpro to fold into alternative conformations. Substitution of only two residues (K269R and R270K) of the eight‐amino‐acid signature in PVY^N HCpro was needed to convert the three‐dimensional (3D) model of PVY^N HCpro to a PVY^O‐like conformation and render PVY^N avirulent in the presence of Ny_tbr, whereas four amino acid substitutions were necessary to change PVY^O HCpro to a PVY^N‐like conformation. Hence, the HCpro conformation rather than other features ascribed to the sequence were essential for recognition by Ny_tbr. The 3D model of PVY^C HCpro closely resembled PVY^O, but differed from PVY^N HCpro. HCpro of all strains was structurally similar to β‐catenin. Sixteen PVY^N605‐based chimeras were inoculated to potato cv. Pentland Crown (Ny_tbr), King Edward (Nc_tbr) and Pentland Ivory (Ny_tbr/Nc_tbr). Eleven chimeras induced necrotic local lesions and caused no systemic infection, and thus differed from both parental viruses that infected King Edward systemically, and from PVY^N605 that infected Pentland Crown and Pentland Ivory systemically. These 11 chimeras triggered both Ny_tbr and Nc_tbr and, in addition, six induced veinal necrosis in tobacco. Further, specific amino acid residues were found to have an additive impact on necrosis. These results shed new light on the causes of PVY‐related necrotic symptoms in potato.     

Interactions and biocontrol of pathogenic Streptomyces strains co-occurring in potato scab lesions

Aims:  To test interactions between pathogenic strains of Streptomyces turgidiscabies , S. scabies and S. aureofaciens . To study biological control of S. turgidiscabies and S. scabies using the nonpathogenic Streptomyces strain (346) isolated from a scab lesion and a commercially available biocontrol agent ( S. griseoviridis strain K61; 'Mycostop').
Methods and Results:  Pathogenic strains of S. turgidiscabies and S. aureofaciens inhibited growth of S. scabies in vitro , whereas strain 346 and S. griseoviridis inhibited the pathogenic strains and were subsequently tested for control of scab in the greenhouse and field. Strains 346 and K61 suppressed development of common scab disease caused by S. turgidiscabies in the greenhouse. Strain 346 reduced incidence of S. turgidiscabies in scab lesions on potato tubers in the field.
Conclusions:  Streptomyces turgidiscabies shows antagonism against S. scabies that occurs in the same scab lesions and shares the ecological niche in the field. Biocontrol of S. turgidiscabies is possible with nonpathogenic Streptomyces strains but interactions may be complicated.
Significance and Impact of the Study:  Streptomyces turgidiscabies may have potential to displace S. scabies under the Scandinavian potato growing conditions. Biological control of the severe potato scab pathogen, S. turgidiscabies , is demonstrated for the first time. The results can be applied to enhance control of common scab.     

Transient coexpression of individual genes encoded by the triple gene block of potato mop-top virus reveals requirements for TGBp1 trafficking

TGBp1, TGBp2, and TGBp3, three plant virus movement proteins encoded by the "triple gene block" (TGB), may act in concert to facilitate cell-to-cell transport of viral RNA genomes. Transient expression of Potato mop-top virus (genus Pomovirus) movement proteins was used as a model to reconstruct interactions between TGB proteins. In bombarded epidermal cells of Nicotiana benthamiana, green fluorescent protein (GFP)-TGBp1 was distributed uniformly. However, in the presence of TGBp2 and TGBp3, GFP-TGBp1 was directed to intermediate bodies at the cell periphery, and to cell wall-embedded punctate bodies. Moreover, GFP-TGBp1 migrated into cells immediately adjacent to the bombarded cell. These data suggest that TGBp2 and TGBp3 mediate transport of GFP-TGBp1 to and through plasmodesmata. Mutagenesis of TGBp1 suggested that the NTPase and helicase activities of TGBp1 were not required for its transport to intermediate bodies directed by TGBp2 and TGBp3, but these activities were essential for the protein association with cell wall-embedded punctate bodies and translocation of TGBpl to neighboring cells. The C-terminal region of TGBp1 was critical for trafficking mediated by TGBp2 and TGBp3. Mutation analysis also suggested an involvement of the TGBp2 C-terminal region in interactions with TGBp1.     

Molecular detection and characterisation of black raspberry necrosis virus and raspberry bushy dwarf virus isolates in wild raspberries

Virus‐derived small interfering RNAs (siRNAs) were extracted from leaves of wild raspberries (Rubus idaeus) sampled from three different regions in Finland and subjected to deep sequencing. Assembly of the siRNA reads to contigs and their comparison to sequences in databases revealed the presence of the bipartite positive‐sense single‐stranded RNA viruses, raspberry bushy dwarf virus (RBDV, genus Idaeovirus), and black raspberry necrosis virus (BRNV, family Secoviridae) in 19 and 26 samples, respectively, including 15 plants coinfected with both viruses. Coverage with siRNA reads [21 and 22 nucleotides (nt)] was higher in BRNV‐FI (Finland) RNA1 (79%) than RNA2 (45%). In RBDV, the coverage of siRNA reads was 89% and 90% for RNA1 and RNA2, respectively. Average depth of coverage was 1.6–4.9 for BRNV and 16.5–36.5 for RBDV. PCR primers designed for RBDV and BRNV based on the contigs were used for screening wild raspberry and a few cultivated raspberry samples from different regions. Furthermore, the sequences of BRNV RNA1 and RNA2 were determined by amplification and sequencing of overlapping contigs (length 1000–1200 nt) except for the 3′ and 5′ ends of RNA1 and RNA2 covered by primers. RNA1 of the Finnish BRNV isolate (BRNV‐FI) was 80% and 86% identical to BRNV‐NA (USA) and BRNV‐Alyth (UK), respectively, whereas the identity of NA and Alyth was 79%. RNA2 of BRNV‐FI was 84% and 80% identical to BRNV‐NA and BRNV‐Alyth, respectively, whereas NA and Alyth were 82% identical. Hence, the strains detected in Finland differ from those reported in the UK and USA. Our results reveal the presence of BRNV in Finland for the first time. The virus is common in wild raspberries and nearly identical isolates are found in cultivated raspberries as well. The results show that wild raspberries in Finland are commonly infected with RBDV or BRNV or both viruses and thus are likely to serve as reservoirs of RBDV and BRNV for cultivated Rubus spp.     

Mapping of the gene Nxphu that controls hypersensitive resistance to potato virus X in Solanum phureja IvP35

 The line IvP35 of the diploid (2n=2x=24) cultivated potato species Solanum phureja (family Solanaceae) expresses hypersensitive resistance (H) to potato X potexvirus (PVX). In this study, a diploid potato population was produced using IvP35 as the male parent and a diploid line of S. tuberosum (87HW13.7) as the female parent and tested for resistance to PVX. Data indicated that H to PVX in IvP35 is a dominant, monogenically inherited trait controlled by a single gene, named Nx _phu , that is in a simplex condition (Nxnx). RFLP analysis carried out on the progeny lines revealed 4 markers (CT220, TG328, CT112 and TG424) from the long arm of chromosome IX that were linked to the hypersensitive phenotype; the closest linkage was observed with the marker TG424. Previous authors have shown that the same region of chromosome IX contains the gene Sw-5 for resistance to tomato spotted wilt tospovirus in Lycopersicon peruvianum (Solanaceae). Received: 18 September 1997 / Accepted: 24 November 1997     

Predator mimicry,not conspicuousness,explains the efficacy of butterfly eyespots

Large conspicuous eyespots on butterfly wings have been shown to deter predators. This has been traditionally explained by mimicry of vertebrate eyes, but recently the classic eye-mimicry hypothesis has been challenged. It is proposed that the conspicuousness of the eyespot, not mimicry, is what causes aversion due to sensory biases, neophobia or sensory overloads. We conducted an experiment to directly test whether the eye-mimicry or the conspicuousness hypothesis better explain eyespot efficacy. We used great tits (Parus major) as model predator, and tested their reaction towards animated images on a computer display. Birds were tested against images of butterflies without eyespots, with natural-looking eyespots, and manipulated spots with the same contrast but reduced resemblance to an eye, as well as images of predators (owls) with and without eyes. We found that mimetic eyespots were as effective as true eyes of owls and more efficient in eliciting an aversive response than modified, less mimetic but equally contrasting eyespots. We conclude that the eye-mimicry hypothesis explains our results better than the conspicuousness hypothesis and is thus likely to be an important mechanism behind the evolution of butterfly eyespots.