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51.
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Meherun Naher Keiichi Motohash Hideki Watanabe Yoshiaki Chikuo Masako Senda Haruhisa Suga Clive Brasier Koji Kageyama 《Mycological Progress》2011,10(1):21-31
A new species of Phytophthora was isolated from stem and root rot of chrysanthemum in the Gifu and Toyama prefectures of Japan. The species differs from
other Phytophthora species morphologically, and is characterized by nonpapillate, noncaducous sporangia with internal proliferation, formation
of both hyphal swellings and chlamydospores, homothallic nature, distinctive intercalary antheridia, and funnel-shaped oogonia.
The new species can grow even at 35°C, with an optimum growth temperature of 30°C in V8 juice agar medium. In phylogenetic
analyses based on five nuclear regions (LSU rDNA; genes for translation elongation factor 1α, β-tubulin, 60 S ribosomal protein
L10, and heat shock protein 90), the isolates formed a monophyletic clade. Although the rDNA ITS region shows a high resolution
and has proven particularly useful for the separation of Phytophthora species, it was difficult to align the sequences for phylogenetic analysis. Therefore, ITS region analysis using related
species as defined by the multigene phylogeny was performed, and the topology of the resulting tree also revealed a monophyletic
clade formed by the isolates of the species. The morphological characteristics and phylogenetic relationships indicate that
the isolates represent a new species, Phytophthora chrysanthemi sp. nov. In pathogenicity tests, chrysanthemum plants inoculated with the isolates developed lesions on stems and roots within
3 days, and the symptoms resembled the ones originally observed. Finally, the pathogen’s identity was confirmed by re-isolation
from lesions of infected plants. 相似文献
53.
Takaaki Koma Cheng Huang Olga A. Kolokoltsova Allan R. Brasier Slobodan Paessler 《Journal of molecular biology》2013
Arenaviruses are enveloped, negative-stranded RNA viruses that belong to the family Arenaviridae. This diverse family can be further classified into OW (Old World) and NW (New World) arenaviruses based on their antigenicity, phylogeny, and geographical distribution. Many of the NW arenaviruses are highly pathogenic viruses that cause systemic human infections characterized by hemorrhagic fever and/or neurological manifestations, constituting public health problems in their endemic regions. NW arenavirus infection induces a variety of host innate immune responses, which could contribute to the viral pathogenesis and/or influence the final outcome of virus infection in vitro and in vivo. On the other hand, NW arenaviruses have also developed several strategies to counteract the host innate immune response. We will review current knowledge regarding the interplay between the host innate immune response and NW arenavirus infection in vitro and in vivo, with emphasis on viral-encoded proteins and their effect on the type I interferon response. 相似文献
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Melbourne-Thomas Jess Audzijonyte Asta Brasier Madeleine J. Cresswell Katherine A. Fogarty Hannah E. Haward Marcus Hobday Alistair J. Hunt Heather L. Ling Scott D. McCormack Phillipa C. Mustonen Tero Mustonen Kaisu Nye Janet A. Oellermann Michael Trebilco Rowan van Putten Ingrid Villanueva Cecilia Watson Reg A. Pecl Gretta T. 《Reviews in Fish Biology and Fisheries》2022,32(1):231-251
Reviews in Fish Biology and Fisheries - One of the most pronounced effects of climate change on the world’s oceans is the (generally) poleward movement of species and fishery stocks in... 相似文献
56.
Respiratory syncytial virus (RSV) is a primary cause of severe lower respiratory tract infection in children worldwide. RSV infects airway epithelial cells, where it activates inflammatory genes via the NF-kappaB pathway. NF-kappaB is controlled by two pathways, a canonical pathway that releases sequestered RelA complexes from the IkappaBalpha inhibitor, and a second, the noncanonical pathway, that releases RelB from the 100-kDa NF-kappaB2 complex. Recently we found that the retinoic acid-inducible gene I (RIG-I) is a major intracellular RSV sensor upstream of the canonical pathway. In this study, we surprisingly found that RIG-I silencing also inhibited p100 processing to 52-kDa NF-kappaB2 ("p52"), suggesting that RIG-I was functionally upstream of the noncanonical regulatory kinase complex composed of NIK.IKKalpha subunits. Co-immunoprecipitation experiments not only demonstrated that NIK associated with RIG-I and its downstream adaptor, mitochondrial antiviral signaling (MAVS), but also showed the association between IKKalpha and MAVS. To further understand the role of the NIK.IKKalpha pathway, we compared RSV-induced NF-kappaB activation using wild type, Ikkgamma(-/-), Nik(-/-), and Ikkalpha(-/-)-deficient MEF cells. Interestingly, we found that in canonical pathway-defective Ikkgamma(-/-) cells, RSV induced RelA by liberation from p100 complexes. RSV was still able to activate IP10, Rantes, and Grobeta gene expression in Ikkgamma(-/-) cells, and this induction was inhibited by small interfering RNA-mediated RelA knockdown but not RelB silencing. These data suggest that part of the RelA activation in response to RSV infection was induced by a "cross-talk" pathway involving the noncanonical NIK.IKKalpha complex downstream of RIG-I.MAVS. This pathway may be a potential target for RSV treatment. 相似文献
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Two enormously destructive pandemics of Dutch elm disease occurred in the 20th century, resulting in the death of a majority of mature elms across much of the northern hemisphere. The first pandemic, caused by Ophiostoma ulmi, occurred as this pathogen spread across Europe, North America and Southwest and Central Asia during the 1920s–1940s. The current pandemic is caused by another Ophiostoma species, O. novo-ulmi. Since the 1940s, O. novo-ulmi has been spreading into the regions previously affected by O. ulmi. It has also spread as two distinct subspecies, termed subsp. americana and subsp. novo-ulmi. This sequence of events has resulted in competitive interactions between these previously geographically isolated pathogens. This article summarizes the biological properties of the Dutch elm disease pathogens and their history of spread. It reviews the remarkable series of genetic events that have occurred during their migrations; including the emergence of genetic clones, the spread of deleterious fungal viruses within the pathogen clones, and the rapid and continuing evolution of O. novo-ulmi via horizontal gene flow. The wider role of horizontal gene flow in the evolutionary potential of migratory plant pathogens is discussed. 相似文献
59.
A guanine nucleotide-sensitive adenylate cyclase in the yeast Saccharomyces cerevisiae 总被引:31,自引:0,他引:31
G F Casperson N Walker A R Brasier H R Bourne 《The Journal of biological chemistry》1983,258(13):7911-7914
Adenylate cyclase in particulate extracts of Saccharomyces cerevisiae utilized either MnATP or MgATP as substrate. A mutation in the CYR1 gene, which codes for the catalytic unit of yeast adenylate cyclase (Matsumoto, K., Uno, I., and Ishikawa, T. (1983) Cell 32, 417-423), eliminated utilization of both MgATP and MnATP, indicating that a single enzyme was responsible for both activities. GTP and guanylyl-5'-imidodiphosphate stimulated yeast adenylate cyclase, while a GDP analog, guanosine-5'-O-(2-thiodiphosphate), competitively inhibited this stimulation. Thermal inactivation studies distinguished putative guanine-nucleotide regulatory protein (N) from the catalytic unit (C) of yeast adenylate cyclase. Yeast N, which conferred guanine nucleotide regulation and the ability to utilize MgATP on yeast C, was quickly inactivated by incubation of particulate extracts at 30 degrees C. In contrast, yeast C, which apparently utilized MnATP as substrate in the absence of a functional N protein, resisted inactivation at 30 degrees C. These observations suggested that physically distinct protein components mediated the catalytic activity of yeast adenylate cyclase and its regulation by guanine nucleotides. These findings indicate a striking homology between the adenylate cyclase systems of S. cerevisiae and those of vertebrate cells. 相似文献
60.
Tian B Nowak DE Jamaluddin M Wang S Brasier AR 《The Journal of biological chemistry》2005,280(17):17435-17448
Tumor necrosis factor (TNF) is a pro-inflammatory cytokine that controls expression of inflammatory genetic networks. Although the nuclear factor-kappaB (NF-kappaB) pathway is crucial for mediating cellular TNF responses, the complete spectrum of NF-kappaB-dependent genes is unknown. In this study, we used a tetracycline-regulated cell line expressing an NF-kappaB inhibitor to systematically identify NF-kappaB-dependent genes. A microarray data set generated from a time course of TNF stimulation in the presence or absence of NF-kappaB signaling was analyzed. We identified 50 unique genes that were regulated by TNF (Pr(F)<0.001) and demonstrated a change in signal intensity of+/-3-fold relative to control. Of these, 28 were NF-kappaB-dependent, encoding proteins involved in diverse cellular activities. Quantitative real-time PCR assays of eight characterized NF-kappaB-dependent genes and five genes not previously known to be NF-kappaB-dependent (Gro-beta and-gamma, IkappaBepsilon, interleukin (IL)-7R, and Naf-1) were used to determine whether they were directly or indirectly NF-kappaB regulated. Expression of constitutively active enhanced green fluorescent.NF-kappaB/Rel A fusion protein transactivated all but IL-6 and IL-7R in the absence of TNF stimulation. Moreover, TNF strongly induced all 12 genes in the absence of new protein synthesis. High probability NF-kappaB sites in novel genes were predicted by binding site analysis and confirmed by electrophoretic mobility shift assay. Chromatin immunoprecipitation assays show the endogenous IkappaBalpha/epsilon, Gro-beta/gamma, and Naf-1 promoters directly bound NF-kappaB/Rel A in TNF-stimulated cells. Together, these studies systematically identify the direct NF-kappaB-dependent gene network downstream of TNF signaling, extending our knowledge of biological processes regulated by this pathway. 相似文献