bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Occurrence of Downy Mildew on Boxleaf Veronica Caused by Peronospora grisea in Italy
Authors: Polizzi G. , Vitale A. , Parlavecchio G. 
Published: May 2007

Boxleaf veronica (Hebe buxifolia (Benth.) Cockayne & Allan), native to New Zealand, is an annual or perennial shrub widely cultivated in Mediterranean zones. During late spring 2003, after seasonably wet and cool weather, a downy mildew epidemic occurred on potted, overhead irrigated, 1-year-old seedlings at a commercial nursery in eastern Sicily (southern Italy). Infections affected boxleaf veronica at first, but spread to variegated boxleaf (H. buxifolia cv. variegata). Initial symptoms on the upper side of leaves were small, gray brown patches that gradually spread, eventually resulting in necrosis in the center of infected areas. At that point, brown patches were evident on both sides of the leaves. Lesions on the lower leaf surface became covered with a fairly dense, pale gray-to-brown layer of conidia and conidiophores. As the disease progressed, these spots coalesced into large and conspicuous brown lesions. The youngest, most succulent shoots withered and died. The large brown lesions on the leaves were disfiguring and affected 95 to 100% of plants in the nursery. All diseased nursery stock had to be discarded. Oospores were not observed in leaf tissues. The fungus recovered from leaves with abundant gray brown sporulation was identified as Peronospora grisea (Unger) Unger. Microscopic observations revealed conidiophores that branched dichotomously five to seven times with branch ends 6 to 10 × 2 to 3 μm, slightly curved, and tapered to a blunt apex. Hyaline conidia were ellipsoid, brownish when mature, and measured 23 to 27 × 15 to 18 μm (mean = 25.2 × 17.1 μm), falling within the range of those reported for P. grisea (1). Pathogenicity was confirmed by inoculating 10 1-yr-old seedlings (10 cm tall) by gently pressing infected leaves with abundant sporulation onto healthy leaves and maintaining inoculated plants in a humid chamber at 21°C. An equal number of noninoculated plants served as controls. After 9 to 11 days, symptoms similar to those originally observed developed onto inoculated plants, and after 12 to 15 days, grayish mildew grew on leaves. Microscopic examination of the developing mycelium confirmed that leaves were infected with P. grisea. Uninoculated control plants did not develop any symptoms. The disease was also confirmed in this way on variegated boxleaf veronica (H. buxifolia cv. variegata). Downy mildew of Hebe spp. has been recorded in New Zealand, Britain, France, Germany, and more recently, West Sussex (2). Heavy rainfall during the spring of 2003 in eastern Sicily could have favored disease development. To our knowledge, this is the first report of downy mildew of boxleaf veronica and variegated boxleaf veronica caused by P. grisea in Italy. References: (1) S. M. Francis and A. M. Berrie. Peronospora grisea. No. 766 in: Descriptions of pathogenic fungi and bacteria. CMI, Kew, Surrey, UK. 1983. (2) J. M. Whipps and C. A. Linfield. Plant Pathol. 36:216, 1987.
First Report of Powdery Mildew Caused by Oidium Subgenus Pseudoidium on Salvia scabra in Italy
Authors: Garibaldi A. , Minuto A. , Bertetti D. , Gullino M. L. 
Published: May 2007

Salvia scabra Thunb. is grown and used on the Italian Riviera as a potted plant and used in gardens. During the spring of 2003, severe outbreaks of a previously unknown powdery mildew were observed in a collection of Salvia spp. maintained at an experimental station at Albenga (northern Italy). Powdery mildew was observed only on S. scabra. Leaves were covered with white exophytic mycelia on both surfaces. As the disease progressed, infected leaves turned yellow and died. Conidia were single, hyaline, cylindric, and measured 21.3 to 35.5 × 12.5 to 22.5 μm (average 28.2 × 18.4 μm). Observations made with a light microscope revealed that foot cells were cylindric and appressoria lobed. Cleistothecia were not observed. The pathogen was identified as Oidium subgenus Pseudoidium (1,2), and pathogenicity was confirmed by gently pressing diseased leaves onto mature leaves of healthy, 40-day-old S. scabra plants. Five plants of S. scabra were used as replicates. Noninoculated plants served as controls. Inoculated and noninoculated plants were maintained in a growth chamber at 20°C. After 5 days, typical symptoms of powdery mildew developed on inoculated plants. Noninoculated plants did not show symptoms. To our knowledge, this is the first report of the presence of powdery mildew on S. scabra in Italy as well as in the world. Erysiphe polygoni DC. (Oidium subgenus Pseudoidium) and E. cichoracearum DC. (Oidium subgen us Reticuloidium) were previously reported as causal agents of powdery mildew on other species of Salvia (S. officinalis and S. sclarea) (3,4). Specimens of this disease are available at the DIVAPRA Collection at the University of Torino. References: (1) R. Belanger et al., eds. The Powdery Mildew A Comprehensive Treatise. The American Phytopathological Society, St Paul, MN, 2002. (2) U. Braun. Nova Hedwigia. 89:700, 1987. (3) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St Paul, MN, 1989. (4) A. Pisi and M. G. Bellardi. Inf. Fitopatol. 48(10):57, 1998.
First Report of Zucchini yellow mosaic virus in Cucumber (Cucumis sativus) in India
Authors: Verma Raj , Prakash Satya , Tomer S. P. S. 
Published: May 2007

In August of 2002, cucumber (Cucumis sativus L. cv. Himangi) plants grown in commercial fields in Pune, western Maharashtra, India, exhibited chlorotic spots, veinal chlorosis, mosaic, blister formation and shoestring symptoms on leaves, stunted growth, and distortion of fruits. Incidence of virus infection in the fields varied from 25 to 38%. Crude sap extracted from infected cucumber leaf samples was inoculated mechanically onto cucumber and indicator host plants. The inoculated glasshouse-grown cucumber plants showed virus symptoms similar to those observed in the field. The virus produced chlorotic local lesions on Chenopodium amaranticolor and chlorotic spots followed by veinal chlorosis, mosaic, vein banding, and leaf distortion on Citrullus lanatus, C. melo, C. sativus, Cucurbita maxima, Cucurbita pepo, Luffa acutangula, and Trichosanthes anguina. The virus did not infect Nicotiana benthamiana, N. glutinosa, and N. tabacum cv. White Burley (1,2). Cucumber and indicator plants were tested using direct antigen coating enzyme-linked immunosorbent assays. A positive reaction was obtained with monoclonal antiserum to Zucchini yellow mosaic virus (ZYMV) but not with antisera to Papaya ringspot virus-P, Cucumber mosaic virus, and Watermelon mosaic virus (Agdia, Inc., Elkhart, IN). The disease was observed again in the field during July to September 2003. Natural infection of zucchini (Cucurbita pepo) by ZYMV has been reported previously from India (3). To our knowledge, this is the first report of ZYMV in cucumber in India. References: (1) H. Pospieszny et al. Plant Dis. 87:1399, 2003. (2) R. Provvidenti et al. Plant Dis. 68:443, 1984. (3) S. J. Singh et al. Indian Phytopathol. 56:174, 2003.
Rubber Tree (Hevea brasiliensis) Bark Necrosis Syndrome I: Still No Evidence of a Biotic Causal Agent
Authors: Pellegrin F. , Nandris D. , Chrestin H. , Duran-Vila N. 
Published: May 2007

The main constraint in rubber plantations worldwide is the cessation of latex production because of two syndromes: (i) tapping panel dryness (TPD), a reversible physiological response to overexploitation; and (ii) bark necrosis (BN), an irreversible syndrome spreading from the collar toward the tapping cut. Early BN symptoms develop in the inner phloem tissues but never affect the cambium. Necrotic patches appear in the outer phloem, inducing bark cracking and peeling, but these alterations never lead to tree death. BN spreads gradually to neighboring rubber trees, and evidence of linear disease centers suggest that a pathogen may be involved, possibly transmitted by the tapping knife. Several previous etiological investigations (fungi, phytoplasma, bacteria, and virus) were performed (3) on leaves, bark, and latex using different methods (e.g., isolation, transmission, chemical treatments, and optic and electron microscope studies). Recent works focused on mechanically transmissible pathogens, such as viroid (2) or virus/double strand RNA, using RNA extraction (nonionic cellulose and appropriate ethanol concentrations) and treatment with RNase A, followed with sequential polyacrylamide gel electrophoresis (s-PAGE), reverse transcription-polymerase chain reaction (RT-PCR), degenerate oligonucleotide primer-PCR (DOP-PCR), and cloning and sequence analysis. While numerous viroid-like (between 250 and 400 nucleotides) and double strand virus-like (1,800 bp) low-molecular-weight RNAs were observed, no definite correlation was found with the BN status of trees. Sequencing of the various isolated RNAs only identified plasmids, nonpathogenic bacteria and yeasts, but none of the suspected pathogens. In addition, previous and recent transmission trials (tapping knife disinfection, bud grafting, bark implantation, and etc.) failed to confirm the involvement of a biotic agent. In conclusion, since these etiological investigations were inconclusive, a physiological disease is now suspected that involves exogenous stresses, nonoptimal vascular relations at the rootstock/scion junction and impaired cyanide metabolism (1,4). References: (1) H. Chrestin et al. Plant Dis. 88:1047, 2004. (2) N. Duran-Vila et al. J. Gen. Virol. 69:3069, 1988. (3) D. Nandris et al. Eur. J. For. Pathol. 21:340, 1991. (4) D. Nandris et al. Plant Dis. 88:1047, 2004.
An Outbreak of Bacterial Speck Caused by Pseudomonas syringae pv. tomato on Tomato Transplants Grown in Commercial Seedling Companies Located in the Western Mediterranean Region of Turkey
Authors: Basim H. , Basim E. , Yilmaz S. , Dickstein E. R. , Jones J. B. 
Published: May 2007

A serious outbreak of a leaf spot disease was observed on tomato transplants grown in commercial seedling companies in southwestern Turkey (Antalya) during the springs of 2002 and 2003. Disease incidence was more severe in the western Mediterranean Region of Turkey. Occurrence of the outbreak resulted in approximately 20 and 25% seedling losses in the springs of 2002 and 2003, respectively. The initial symptoms consisted of pronounced water-soaked, dark brown-to-black spots on young expanding leaves that were 1 to 2 mm in diameter. Later, a number of leaf spots on older leaves enlarged and coalesced, causing leaf desiccation and finally, seedling death. In addition, in 2003 the disease incidence was approximately 5% in 142 commercial greenhouses. Tomato production was unaffected since significant outbreaks did not occur on greenhouse plants. No fruit symptoms were observed. Twenty-six strains were isolated from diseased tomato seedlings and plants from different greenhouses located in different places and all were gram negative and fluorescent on King's B medium. All strains were levan and gelatin liquefaction positive and oxidase and arginine dihydrolase negative. None of the 26 strains utilized erythritol and l-lactate as the sole carbon source (1,2). Fatty acid analysis identified the strains as Pseudomonas syringae pv. tomato with similarity indices ranging from 0.876 to 0.932%. Pathogenicity of the isolates was confirmed on 4-week-old tomato seedlings (cv. Biotek Selin) sprayed with the bacterial suspensions containing 108 CFU/ml of sterile water. Later, a number of leaf spots on the leaves enlarged and coalesced, causing leaf desiccation. Inoculated and control tomato seedlings were covered with polyethylene bags and placed in a growth chamber at 25°C for 48 h and then the bags were removed. Small (1 to 2 mm), water-soaked, dark brown-to-black spots similar to those observed in the greenhouses of commercial seedling companies and commercial greenhouses that produce tomato developed on the young expanding leaves of inoculated plants within 7 to 10 days. No symptoms developed on control plants. The bacterium was reisolated from inoculated plants and identified as a strain of Pseudomonas syringae pv. tomato. Koch's postulates were fulfilled. To our knowledge, this is the first report for the occurrence and outbreak of the bacterial speck disease on tomato transplants in greenhouses of commercial tomato seedling production companies in Turkey. References: (1) D. C. Hildebrand et al. Pages 60–80 in: Laboratory Guide for Identification of Plant Pathogenic Bacteria. N. D. Schaad, ed. The American Phytopathological Society, 1988. (2) J. B. Jones et al. Plant Dis. 70:151, 1986.
Phylogeny, evolution and systematics of Moehringia (Caryophyllaceae) as inferred from molecular and morphological data: a case of homology reassessment
Authors: Fior Simone , Karis Per Ola 
Published: May 2007

AbstractThe phylogeny of the genus Moehringia (Caryophyllaceae) is investigated by means of analyzing nuclear (ITS) and chloroplast (matK) sequence data in combination with morphological characters. Parsimony and Bayesian methods yield consistent results, and a common phylogenetic signal is shared by the nuclear and chloroplast data. Morphological characters are affected by a high level of homoplasy, but they provide valuable information when analyzed in combination with the molecular data. Moehringia is paraphyletic to Arenaria with the Iberian taxa belonging to Moehringia sect. Pseudomoehringia McNeill more closely related to Arenaria. This cladistic evidence led us to reinterpret the homology of the key character used in most, if not all, floras, to separate Moehringia from Arenaria, i.e., the seed strophiole. Thorough anatomical studies were carried out to elucidate the ontogeny of the strophiole, which proved different in Moehringia s. str. and the Iberian taxa. Within Moehringia s. str., two sister clades are recognized (i.e., Moehringia sect. Moehringia and M. sect. Latifoliae much as recognized by McNeill, whereas representatives of M. sect. Diversifoliae are assigned to either groups), and biogeographical events related to the Würm glaciation are considered to play a fundamental role in the evolution and present distribution of the genus. The variation of the strophiole is regarded as adaptability to ecological conditions and dispersal agents. We also propose two new combinations and two replacement names: Arenaria glochidisperma (J.M. Mont.) Fior et P.O. Karis, comb. nov., Arenaria tejedensis (Willk.) Fior et P.O. Karis, comb. nov., Arenaria suffruticosa Fior et P.O. Karis, nom. nov. for Moehringia intricata Willk., and Arenaria funiculata Fior et P.O. Karis, nom. nov. for Moehringia fontqueri Pau.© The Willi Hennig Society 2007.
Critical role for D‐type cyclins in cellular transformation induced by E6/E7 of human papillomavirus type 16 and E6/E7/ErbB‐2 cooperation
Authors: Yasmeen Amber , Hosein Abdel N. , Yu Qunyan , Al Moustafa Ala‐Eddin 
Published: May 2007

Recently, we reported that E6/E7 of human papillomavirus (HPV) type 16 cooperates with the ErbB‐2 receptor to induce cellular transformation of human normal oral epithelial (NOE) and mouse normal embryonic fibroblast (NEF) cells. Furthermore, we demonstrated that cyclin D1 is essential for this transformation induced by E6/E7 and E6/E7/ErbB‐2 cooperation using cyclin D1 antisense and knockout (D1−/–) cells. To determine the role of all D‐type cyclins (D1, D2 and D3) in E6/E7/ErbB‐2 cooperation, we examined the effects of E6/E7, ErbB‐2 alone and E6/E7/ErbB‐2 together in NEF, NEF‐D1−/–, NEF‐D2−/– and NEF‐D3−/– cells. We confirm that NEF‐E6/E7 and NEF‐E6/E7/ErbB‐2, but not NEF‐ErbB‐2 cells, induce colony formation in soft agar and tumor formation in nude mice. We report that E6/E7, ErbB‐2 and E6/E7/ErbB‐2 together all fail to induce neoplastic transformation of D1−/– and D2−/– cells in vitro and in vivo. In contrast, E6/E7/ErbB‐2 together but neither E6/E7 nor ErbB‐2 alone provoke cellular transformation of D3−/– cells. Nevertheless, D3−/–E6/E7/ErbB‐2 cells resulted in up to a 60 and 50% decrease in colony and tumor formation in soft agar and nude mice, respectively, compared with NEF‐E6/E7/ErbB‐2 cells. Furthermore, using cyclin D2 small interfering RNA we inhibited tumor and colony formation of the human NOE‐E6/E7‐ErbB‐2‐transformed cell line; in contrast, cyclin D3 small interfering RNA repressed approximately 50% of colony and 40% of tumor formation of E6/E7/ErbB‐2 cooperation in this cell line. These data suggest that cyclins D1, D2 and D3 (to a lesser extent) are important downstream mediators of the cellular transformation induced by E6/E7 and E6/E7/ErbB‐2 cooperation in normal cells. Our data imply that anti‐D‐type cyclin therapies are important in the treatment of human cancers expressing high‐risk HPV or HPV/ErbB‐2. (Cancer Sci 2007; 98: 973–977)
Gene–gene and gene–environment interactions between alcohol drinking habit and polymorphisms in alcohol‐metabolizing enzyme genes and the risk of head and neck cancer in Japan
Authors: Hiraki Akio , Matsuo Keitaro , Wakai Kenji , Suzuki Takeshi , Hasegawa Yasuhisa , Tajima Kazuo 
Published: May 2007

Alcohol consumption is a strong risk factor for squamous cell carcinoma of the head and neck (SCCHN). The genetic polymorphisms aldehyde dehydrogenase2 (ALDH2) Glu487Lys and alcohol dehydrogenase 2 (ADH2) His47Arg, which have a strong impact on alcohol metabolism, are common in the Japanese population. To clarify the significance of these polymorphisms in SCCHN carcinogenesis, we conducted a matched case‐control study with 239 incident SCCHN subjects and 716 non‐cancer controls. Both ADH2 Arg/Arg and ALDH2 Glu/Lys were found to be independently associated with increased risk, with odds ratios (OR) of 2.67 (95% confidence interval [CI] 1.51–4.57) and 1.66 (95% CI 1.20–2.31), respectively. Further, compared with subjects having both ADH2 His/His and ALDH2 Glu/Glu, the adjusted OR and its 95% CI for those with both ADH2 Arg/Arg and ALDH2 Glu/Lys was 5.00 (2.32–10.71) in all subjects. This combination effect was evident in heavy drinkers (OR 11.3, 95% CI 2.97–43.3) but not in moderate or non‐drinkers. Statistically significant gene–environment interactions between the two polymorphisms and drinking level were seen (ADH2 P = 0.035, ALDH2, P = 0.013). Furthermore, we also found a statistically significant gene–gene interaction between the two polymorphisms (P = 0.042). In conclusion, this case‐control study showed a significantly increased risk of SCCHN in subjects with the ADH2 Arg/Arg and ALDH2 Glu/Lys polymorphisms in a Japanese population. In addition, our results also demonstrated that this risk was associated with significant gene–gene interactions between ADH2 and ALDH2 polymorphisms, as well as gene–environment interactions between these polymorphisms and alcohol drinking. (Cancer Sci 2007; 98: 1087–1091)
Studies of a germinal centre B‐cell expressed gene, GCET2, suggest its role as a membrane associated adapter protein
Authors: Pan Zenggang , Shen Yulei , Ge Baosheng , Du Cheng , McKeithan Timothy , Chan Wing C 
Published: May 2007

Summary GCET2 (Germinal centre B‐cell expressed transcript 2; also named HGAL) is a newly cloned gene that has been shown to be a useful marker for germinal centre (GC) B cells and GC B‐cell derived malignancies, including follicular lymphomas and germinal centre B cell‐like diffuse large B‐cell lymphomas (GCB‐DLBCLs), and is a useful prognosticator for DLBCLs. We report here the biochemical and biological properties of GCET2, which may help to determine its role in the GC reaction. GCET2 is constitutively localised in the plasma membrane but is excluded from lipid rafts. GCET2 does not have a transmembrane domain, and its membrane localisation is mediated by myristoylation and palmitoylation. GCET2 has five conserved putative tyrosine phosphorylation sites, and it can be phosphorylated following pervanadate treatment in B cells. By serially mutating the five tyrosines, the third and fourth tyrosines were found to be essential for GCET2 phosphorylation. GCET2 was phosphorylated when co‐transfected into COS7 cells with protein tyrosine kinases (PTKs) LYN, LCK or SYK, and therefore it could be a substrate of these kinases in B cells. The third tyrosine site (107YENV) of GCET2 is a consensus GRB2 binding site, and GCET2 was found to associate with GRB2 through the third tyrosine following phosphorylation. Our data suggests that GCET2 may be an adaptor protein in GC B cells that transduces signals from GC B‐cell membrane to the cytosol via its association with GRB2.
Gene silencing by DNA methylation in haematological malignancies
Authors: Boultwood Jacqueline , Wainscoat James S. 
Published: May 2007

SummaryThe past decade has seen an explosion of interest in the epigenetics of cancer, with an increasing understanding that this form of genomic modification plays a critical role in pathogenesis. The malignant phenotype results from a step‐wise increase of both genetic abnormalities and epigenetic modifications, leading to dysregulation of critical genes controlling cell growth, differentiation and apoptosis. The methylation of CpG islands within gene promoters is a major epigenetic transcriptional control mechanism that is frequently dysregulated in human cancer. This phenomenon (methylation of CpG islands) plays a critical role in the transcriptional silencing of tumour suppressor genes in cancer and has prompted the development and testing of several demethylating agents aimed at reversing this process. Clinical trials using epigenetically targeted therapies have yielded particularly promising results in the myelodysplastic syndromes (MDS), in which tumour suppressor gene silencing by promoter methylation is a frequent event. Several genes and gene pathways disrupted by aberrant CpG island methylation have now been identified in haematological malignancies, the most frequently studied being the cell cycle inhibitors p16 (now termed CDKN2A; mostly methylated in lymphoid malignancy) and p15 (now termed CDKN2B; commonly methylated in lymphoid and myeloid malignancies). This review will discuss the role that aberrant gene silencing by promoter hypermethylation plays in the molecular pathogenesis of haematological malignancies and assess the clinical potential of demethylating agents for the management of patients.