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Japanese star anise (Illicium anisatum L., JSA) is seriously damaged by a ringspot disease in Japan. Herein, to determine the causal agent using high-throughput sequencing, we discovered viral RNAs associated with JSA ringspot disease. We then determined the complete or near-complete nucleotide sequences of these RNAs using Sanger sequencing and RACE. The complementary strand of viral RNAs 1, 2, 3, 4, and 5 encoded a single protein, which shared sequence identity with P1 (RNA-dependent RNA polymerase), P2 (glycoprotein precursor), P3 (nucleocapsid protein), P4 (movement protein), and a protein with unknown function of emaraviruses (genus Emaravirus), respectively; however, the highest amino acid sequence identity for the P1–P5 proteins between JSARaV and known emaraviruses was 41.9%, 30.0%, 30.1%, 52.2%, and 38.0%, respectively, all of which were lower than the species demarcation criterion. Furthermore, RNA segments harbored conserved 12-nt terminal sequences at the 5′- and 3′-termini, and a high complementarity of approximately 20 nt in 5′- and 3′-terminal sequences. Transmission electron microscopy confirmed the presence of virus-like particles. JSA ringspot disease was found to be transmitted by an eriophyid mite (subclass Acari, superfamily Eriophyoidea) that belongs to the family Diptilomiopidae. Taken together, these results identified the virus responsible for the ringspot disease of JSA as a new member of the genus, Emaravirus, which we named as the Japanese star anise ringspot-associated virus (JSARaV). Moreover, this is the first report noting that eriophyid mites of the family Diptilomiopidae are capable of transmitting emaravirus.

In July 2018, pepper plants (Capsicum annuum L.) with chlorotic leaves and fruits were observed in Kochi prefecture, Japan. High-throughput sequencing (HTS) identified the possible presence of an ophiovirus-like virus possessing three RNA segments in a chlorotic leaf. Using Sanger sequencing with primers designed based on the HTS results and a different source of RNA from the one used for HTS, the complete nucleotide sequences of three RNA segments encoding four proteins on their complementary strand were determined. The amino acid sequences of these four proteins showed similarity to those of the RNA-dependent RNA polymerase, RNA-silencing suppressor protein, movement protein, and coat protein, respectively, of ophioviruses, which are negative-sense single-stranded RNA viruses. However, the coat protein amino acid sequence of the virus found on pepper plants was no more than 61.9% identical to those of any known ophioviruses, which is lower than the species demarcation threshold of 85 %. Hence, we suggest that this virus, which we have named "pepper chlorosis associated virus" (PepCaV) should be considered a member of a new species in the genus Ophiovirus, for which we propose the name "Ophiovirus capsici". The results of phylogenetic analysis using coat protein amino acid sequences of PepCaV and other ophioviruses also supported this conclusion. PepCaV RNA was found to have conserved nucleotide sequences at both the 5' and 3' termini of the different RNA segments, and the conserved terminal nucleotide sequences were predicted to form a self-complementary double-stranded region, resulting in a panhandle structure in each of the genomic RNAs.

An attenuated mutant strain of melon yellow spot virus (MYSV), an Orthotospovirus, designated as SA08-8, was obtained from a pathogenic isolate, C95S, via high temperature treatment, single local lesion isolation, and serial mechanical inoculation. Under greenhouse conditions, the SA08-8 strain conferred the cross-protection against wild-type MYSV but it was not transmissible by its known natural vector melon thrips. In SA08-8 genome, a total of 16 amino acid substitutions were found in the genes encoding RNA-dependent RNA polymerase, glycoprotein precursor, and nonstructural S protein. This attenuated mutant strain is a potential biocontrol agent for MYSV-induced crop diseases in the field.

Shiso (Perilla frutescens var. crispa) is widely grown as an important vegetable or herb crop in Japan. Beginning around the year 2000, occurrences of severe mosaic symptoms on shiso were documented and gradually spread across Kochi Prefecture, one of four major shiso production areas in Japan. Next generation sequencing and cloning indicated the presence of a previously unknown virus related to the members of the genus Emaravirus, for which we proposed the name Perilla mosaic virus (PerMV). The genome of PerMV consists of 10 RNA segments, each encoding a single protein in the negative-sense orientation. Of these proteins, P1, P2, P3a, P3b, P4, and P5 show amino acid sequence similarities with those of known emaraviruses, whereas no similarities were found in P6a, P6b, P6c, and P7. Characteristics of the RNA segments as well as phylogenetic analysis of P1 to P4 indicate that PerMV is a distinct and highly divergent emaravirus. Electron microscopy observations and protein analyses corresponded to presence of an emaravirus. Transmission experiments demonstrated that an eriophyid mite, Shevtchenkella sp. (family Eriophyidae), transmits PerMV with a minimum 30-min acquisition access period. Only plants belonging to the genus Perilla tested positive for PerMV, and the plant−virus−vector interactions were evaluated. The nucleotide sequences reported here are available in the DDBJ/ENA/GenBank databases under accession numbers LC496090 to LC496099.

In June 2017, sweet pepper plants showing chlorosis in leaves and fruits were observed in Susaki City, Kochi Prefecture, Japan. We had named the disease pepper chlorosis (Tairyoku-byo). A phytoplasma was observed by electron microscopy and identified as ‘Candidatus Phytoplasma solani’, based on homology searches and molecular phylogeny using nucleotide sequences of 16S rDNA. To our knowledge, this is the first report showing the occurrence of ‘Ca. P. solani’ in Japan.

Unfortunately, the inclusion of original names (in non-Latin script) of the following authors caused problems with author name indexing in PubMed. Therefore, these original names were removed from XML data to correct the PubMed record. Mengji Cao, Yuya Chiaki, Hideki Ebihara, Jingjing Fu, George Fú Gāo, Tong Han, Jiang Hong, Ni Hong, Seiji Hongo, Masayuki Horie, Dàohóng Jiāng, Fujio Kadono, Hideki Kondō, Kenji Kubota, Shaorong Li, Longhui Li, Jiànróng Lǐ, Huazhen Liu, Tomohide Natsuaki, Sergey V. Netesov, Anna Papa, Sofia Paraskevopoulou, Liying Qi, Takahide Sasaya, Mang Shi, Xiǎohóng Shí, Zhènglì Shí, Yoshifumi Shimomoto, Jin‑Won Song, Ayato Takada, Shigeharu Takeuchi, Yasuhiro Tomitaka, Keizō Tomonaga, Shinya Tsuda, Changchun Tu, Tomio Usugi, Nikos Vasilakis, Jiro Wada, Lin‑Fa Wang, Guoping Wang, Yanxiang Wang, Yaqin Wang, Tàiyún Wèi, Shaohua Wen, Jiangxiang Wu, Lei Xu, Hironobu Yanagisawa, Caixia Yang, Zuokun Yang, Lifeng Zhai, Yong‑Zhen Zhang, Song Zhang, Jinguo Zhang, Zhe Zhang, Xueping Zhou. In addition, the publication call-out in the supplementary material was updated from issue 11 to issue 12. The original article has been corrected.

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Some isolates of Corynespora cassiicola from eggplant leaves with black blight can also cause Corynespora blight on sweet pepper. To differentiate eggplant isolates differing in virulence to sweet pepper, we first created two sets of primers based on nucleotide sequences of DNA fragments specific to virulent and to avirulent isolates, respectively, in a random amplified polymorphic DNA analysis using two random primers. A multiplex polymerase chain reaction using the two primer sets allowed us to discriminate isolates virulent to sweet pepper from among eggplant isolates.

Sweet peppers (cv. Tosajishi beauty) with leaf blight symptoms were observed in Kochi Prefecture, 2003. Initially, small spots formed on leaves, and later enlarged to brown to dark brown spots, and eventually blighted leaves fell. Several bacteria that caused the same symptoms were isolated and subsequently reisolated. These bacteria were identified as Pseudomonas cichorii on the basis of bacterial characteristics and the 16S rRNA gene sequence. This is the first report of bacterial leaf blight in the sweet pepper in the world.

In pepper plants (genus Capsicum), the resistance against Tobamovirus spp. is conferred by L gene alleles. The recently identified L variant L(1a) can recognize coat proteins (CPs) of Tobacco mild green mosaic virus Japanese strain (TMGMV-J) and Paprika mild mottle virus Japanese strain (PaMMV-J), but not of Pepper mild mottle virus (PMMoV), as the elicitor to induce resistance at 24 °C. Interestingly, L(1a) gene-mediated resistance against TMGMV-J, but not PaMMV-J, is retained at 30 °C. This observation led us to speculate that L(1a) can discriminate between CPs of TMGMV-J and PaMMV-J. In this study, we aimed to determine the region(s) in CP by which L(1a) distinguishes TMGMV-J from PaMMV-J. By using chimeric CPs consisting of TMGMV-J and PaMMV-J, we found that the chimeric TMGMV-J CP, whose residues in the β-sheet domain were replaced by those of PaMMV-J, lost its ability to induce L(1a) gene-mediated resistance at 30 °C. In contrast, the chimeric PaMMV-J CP with the β-sheet domain replaced by TMGMV-J CP was able to induce L(1a) gene-mediated resistance at 30 °C. Furthermore, viral particles were not detected in the leaves inoculated with either chimeric virus. These observations indicated that the amino acids within the β-sheet domain were involved in both the induction of L(1a) gene-mediated resistance and virion formation. Further analyses using chimeric CPs of TMGMV-J and PMMoV indicated that amino acids within the β-sheet domain alone were not sufficient for the induction of L(1a) gene-mediated resistance by TMGMV-J CP. These results suggest that multiple regions in Tobamovirus CP are implicated in the induction of L(1a) gene-mediated resistance.

The pathogen of black blight of eggplant (Solanum melongena L.) was previously described as Corynespora melongenae Takimoto in Japan, but there was no Latin description of the fungus. We collected the fungus again in Shimane and Kochi prefectures, the western regions of Japan and reidentified them as C. cassiicola based on the morphological characteristics and sequences of rDNA-ITS regions after confirming their pathogenicity on eggplant. We propose to replace C. melongenae Takimoto nom. inval. with C. cassiicola as the pathogen of black blight in eggplant in Japan.

In order to develop a method for discrimination of Corynespora cassiicola isolates pathogenic to sweet pepper among Japanese isolates, this study analysed pathogenic variations of 64 Japanese isolates of C. cassiicola on perilla, cucumber, tomato, aubergine and sweet pepper, and their multigene phylogeny. Japanese isolates were divided into seven pathogenicity groups (PG1–PG7). The virulence of isolates in PG1–PG5 was restricted to perilla, cucumber, tomato, aubergine and sweet pepper, respectively. Isolates in PG6 were virulent to sweet pepper, tomato and aubergine. Isolates in PG7 were avirulent to all tested plants. Multigene phylogenetic analysis of the isolates based on β-tubulin, translation elongation factor 1-α, calmodulin and actin genes showed three divergent clusters, MP-A, MP-B and MP-C. These clusters included all isolates in PG1, PG2, PG8 and PG9 (MP-A), PG3 and PG5 (MP-B) and PG4 and PG6 (MP-C). Isolates in PG7 were distributed amongst all clusters. Furthermore, random amplified polymorphic DNA (RAPD) analysis using universal primers, Q17 (5′-GAAGCCCTTG-3′) and Q13 (5′-GGAGTGGACA-3′), facilitated discrimination of isolates virulent on sweet pepper amongst isolates in MP-B and MP-C, respectively. Together, a combination of the multigene analysis and the RAPD technique allowed the discrimination of the isolates virulent to sweet pepper.

A new disease causing necrotic spots and yellowing on leaves of balsam pear (Momordica charantia) was found in Kochi Prefecture, Japan. In this study, we identified the causal pathogen as Melon yellow spot virus (MYSV) based on morphology of virus particles, serology, and the nucleotide sequence of the nucleocapsid protein gene. This is the first report of natural infection of balsam pear by MYSV. We propose the name spotted wilt for this new disease of balsam pear.

In 2004, Corynesopra cassiicola was isolated from dark brown spots on leaves and fruits and from black blights on stems of sweet pepper plants in Kochi Prefecture, Japan. The isolated fungus was then used to inoculate sweet pepper plants and subsequently reisolated from the plants with dark brown spots and black blights, showing that C. cassiicola is a new pathogen causing Corynespora blight on sweet pepper plants.

In pepper plants (genus Capsicum), the resistance against Tobamovirus spp. is conferred by L gene alleles. The recently identified L variant L(1a) can recognize coat proteins (CPs) of Tobacco mild green mosaic virus Japanese strain (TMGMV‐J) and Paprika mild mottle virus Japanese strain (PaMMV‐J), but not of Pepper mild mottle virus (PMMoV), as the elicitor to induce resistance at 24 °C. Interestingly, L(1a) gene‐mediated resistance against TMGMV‐J, but not PaMMV‐J, is retained at 30 °C. This observation led us to speculate that L(1a) can discriminate between CPs of TMGMV‐J and PaMMV‐J. In this study, we aimed to determine the region(s) in CP by which L(1a) distinguishes TMGMV‐J from PaMMV‐J. By using chimeric CPs consisting of TMGMV‐J and PaMMV‐J, we found that the chimeric TMGMV‐J CP, whose residues in the β‐sheet domain were replaced by those of PaMMV‐J, lost its ability to induce L(1a) gene‐mediated resistance at 30 °C. In contrast, the chimeric PaMMV‐J CP with the β‐sheet domain replaced by TMGMV‐J CP was able to induce L(1a) gene‐mediated resistance at 30 °C. Furthermore, viral particles were not detected in the leaves inoculated with either chimeric virus. These observations indicated that the amino acids within the β‐sheet domain were involved in both the induction of L(1a) gene‐mediated resistance and virion formation. Further analyses using chimeric CPs of TMGMV‐J and PMMoV indicated that amino acids within the β‐sheet domain alone were not sufficient for the induction of L(1a) gene‐mediated resistance by TMGMV‐J CP. These results suggest that multiple regions in Tobamovirus CP are implicated in the induction of L(1a) gene‐mediated resistance.