The halophile Vibrio vulnificus is an etiologic agent of human mortality from seafood-borne infections. We applied whole-genome sequencing and comparative analysis to investigate the evolution of this pathogen. The genome of biotype 1 strain, V. vulnificus YJ016, was sequenced and includes two chromosomes of estimated 3377 kbp and 1857 kbp in size, and a plasmid of 48,508 bp. A super-integron (SI) was identified, and the SI region spans 139 kbp and contains 188 gene cassettes. In contrast to non-SI sequences, the captured gene cassettes are unique for any given Vibrio species and are highly variable among V. vulnificus strains. Multiple rearrangements were found when comparing the 5.3-Mbp V. vulnificus YJ016 genome and the 4.0-Mbp V. cholerae El Tor N16961 genome. The organization of gene clusters of capsular polysaccharide, iron metabolism, and RTX toxin showed distinct genetic features of V. vulnificus and V. cholerae. The content of the V. vulnificus genome contained gene duplications and evidence of horizontal transfer, allowing for genetic diversity and function in the marine environment. The genomic information obtained in this study can be applied to monitoring vibrio infections and identifying virulence genes in V. vulnificus.[Supplemental material is available online at www.genome.org and at http://genome.nhri.org.tw/vv/. The nucleotide sequence data from this study have been submitted to DDBJ/EMBL/GenBank under accession nos. BA000037, BA000038, and AP005352.]Vibrio vulnificus is an etiologic agent for severe human infection acquired through wounds or contaminated seafood. This organism is divided into three biotypes according to their different biochemical and biological properties (Linkous and Oliver 1999). Among them the biotype 1 strains are most frequently isolated from the clinical specimens. Opportunistic infection in susceptible individuals typically causes mortality within 24 to 48 h of the exposure. The bacterium is halophilic, and it is abundantly present in estuarine ecosystems throughout the world. Isolated incidents of V. vulnificus infection have been reported in the U.S.A., Europe, Korea, Taiwan (Park et al. 1991;Chuang et al. 1992;Dalsgaard et al. 1996;Hlady and Klontz 1996), and many other countries. According to CDC statistics, V. vulnificus is a major bacterial cause of mortality associated with food-borne diseases, and it results in the highest death rate of any causative agent (Todd 1989).V. vulnificus belongs to the ␥-group of Proteobacteria, and it shares morphological and biochemical characteristics with other human vibrio pathogens, including Vibrio cholerae and Vibrio parahaemolyticus. Bacteria of the Vibrionaceae family, which show a comma-shape microscopic appearance and a polar flagellum appendage, are mostly aquatic inhabitants that require NaCl for optimal growth. On the basis of clinical and epidemiology studies, diseases associated with V. vulnificus infection have been found to present in two patterns (Blake et al. 1979). In one, primary septicemia occurred in individ...
NPC shows significant upregulation of OSF-2 and downregulation of pIgR. Expression of OSF-2 is likely to play a role in the pathogenesis of NPC. In addition, expression of OSF-2 and pIgR is disassociated with the expression of their regulatory cytokines in NPC biopsy specimens, suggesting that the tumors may have altered responses to certain cytokines.
Increased levels of dysfunctional mitochondria within skeletal muscle are correlated with numerous age‐related physiopathological conditions. Improving our understanding of the links between mitochondrial function and muscle proteostasis, and the role played by individual genes and regulatory networks, is essential to develop treatments for these conditions. One potential player is the mitochondrial outer membrane protein Fis1, a crucial fission factor heavily involved in mitochondrial dynamics in yeast but with an unknown role in higher‐order organisms. By using Drosophila melanogaster as a model, we explored the effect of Fis1 mutations generated by transposon Minos‐mediated integration. Mutants exhibited a higher ratio of damaged mitochondria with age as well as elevated reactive oxygen species levels compared with controls. This caused an increase in oxidative stress, resulting in large accumulations of ubiquitinated proteins, accelerated muscle function decline, and mitochondrial myopathies in young mutant flies. Ectopic expression of Fis1 isoforms was sufficient to suppress this phenotype. Loss of Fis1 led to unbalanced mitochondrial proteostasis within fly muscle, decreasing both flight capabilities and lifespan. Fis1 thus clearly plays a role in fly mitochondrial dynamics. Further investigations into the detailed function of Fis1 are necessary for exploring how mitochondrial function correlates with muscle health during aging.
Decision-making is considered an important aspect of cognitive function. Impaired decision-making is a consequence of cognitive decline caused by various physiological conditions, such as aging and neurodegenerative diseases. Here we exploited the value-based feeding decision (VBFD) assay, which is a simple sensory–motor task, to determine the cognitive status of Drosophila. Our results indicated the deterioration of VBFD is notably correlated with aging and neurodegenerative disorders. Restriction of the mushroom body (MB) neuronal activity partly blunted the proper VBFD. Furthermore, using the Drosophila polyQ disease model, we demonstrated the impaired VBFD is ameliorated by the dinitrosyl iron complex (DNIC-1), a novel and steady nitric oxide (NO)-releasing compound. Therefore we propose that the VBFD assay provides a robust assessment of Drosophila cognition and can be used to characterize additional neuroprotective interventions.
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