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In this study, we sequenced the complete mitochondrial genome of Scaphiodonichthys acanthopterus (Cypriniformes, Cyprinidae). This mitochondrial genome, consisting of 16,612 base pairs (bp), encoded genes for 13 protein-coding genes, two ribosomal RNAs, 22 transfer RNAs, and one non-coding control region as those found in other vertebrates, with the gene order identical to that of typical vertebrates. The control region, of 941 bp in length, is located between tRNA Pro and tRNA Phe. The overall base composition of the heavy strand shows T 25.23%, C 26.85%, A 31.96%, and G 15.95%, with a slight AT bias of 57.19%. [ABSTRACT FROM AUTHOR]

The Onychostoma barbatulus is a small cyprinid fish and distributed mainly in Taiwan and mainland China. The total length of O. barbatulus mitogenome is 16,597 bp, and had a gene content consisting of 13 protein-coding genes, 22 transfer RNAs, 2 ribosomal RNAs genes and a noncoding control region. The determination of O. barbatulus mitogenome would play an important role both in the delineation of phylogeographic history and population genetic structure, as well as reflection of conservation efforts on the genetic diversity and population vitality. [ABSTRACT FROM AUTHOR]

We determined the complete mitochondrial genome (mitogenome) sequence of Onychostoma alticorpus, which is known as an endemic freshwater species in Taiwan, by using long polymerase chain reaction method. The total length of O. alticorpus mitogenome is 16,680 bp, consisting of 13 protein-coding genes, 22 transfer RNAs, 2 ribosomal RNAs genes and a noncoding control region. The overall base composition of O. alticorpus is 30.88% for A, 23.57% for T, 16.56% for G and 28.99% for C, with a slight AT bias of 54.45%. Gene location and specific usage of distinct termination codon types characterize typically the vertebrate mitochondrial genome. The determination of O. alticorpus mitogenome would play an important role not only in the delineation of phylogeographic history and population genetic structure, but reflection of conservation efforts on the genetic diversity as well as population vitality. [ABSTRACT FROM AUTHOR]

Chloroquine (CQ) is an antimalaria drug that has been used in clinical practice for several decades. One serious complication of CQ treatment is the macular retinopathy caused by the disruption of the retinal pigmented epithelium, leading to vision loss. Little is known about how CQ affects retinal pigmented epithelium. In this study, we found that cell proliferation was reduced by CQ treatment in time and dose‐dependent manners. No obvious cell death was detected; however, what was observed instead was G0/G1 arrest during which primary cilium started to grow in the presence of CQ. Pharmacological inhibition of primary cilium formation led to a reduction of cell viability suggesting that CQ‐induced primary cilium protected cells from death. In addition to cell growth, with the CQ treatment the retina pigmented epithelium (RPE) cells less flattened with the spindle‐like protrusion. When checking the microtubule networks, the microtubule nucleation activity was disrupted in the presence of CQ. The level of p150 glued, the largest subunit of dynactin, was reduced in CQ‐treated RPE1 cells, and depletion of p150 glued resulted in a phenotype reminiscent of CQ‐treated cells. Thus, CQ treatment reduced the expression of p150 glued, leading to reduced S phase entry and defective microtubule nucleation. Chloroquine (CQ) treatment reduced the expression of p150glued, leading to reduced S phase entry and defective microtubule nucleation. [ABSTRACT FROM AUTHOR]

Septins play important roles in regulating development and differentiation. Septin 7 (SEPT7) is a crucial component in orchestrating the septin core complex into highly ordered filamentous structures. Here, we showed that genetic depletion of SEPT7 or treatment with forchlorfenuron (FCF; a compound known to affect septin filament assembly) led to reduced the S phase entry in cell models and zebrafish embryos. In addition to colocalizing with actin filaments, SEPT7 resided in the centrosome, and SEPT7 depletion led to aberrant mitotic spindle pole formation. This mitotic defect was rescued in SEPT7‐deficient cells by wild‐type SEPT7, suggesting that SEPT7 maintained mitotic spindle poles. In addition, we observed disorganized microtubule nucleation and reduced cell migration with SEPT7 depletion. Furthermore, SEPT7 formed a complex with and maintained the abundance of p150glued, the component of centriole subdistal appendages. Depletion of p150glued resulted in a phenotype reminiscent of SEPT7‐deficient cells, and overexpression of p150glued reversed the defective phenotypes. Thus, SEPT7 is a centrosomal protein that maintains proper cell proliferation and microtubule array formation via maintaining the abundance of p150glued. [ABSTRACT FROM AUTHOR]

p150(glued) is the largest subunit of dynactin protein complex, through which cargo vesicles link to the microtubule minus-end directed motor protein dynein. In addition, p150(glued) also locates in the mother centriole where it organizes the subdistal appendage. The components of appendage are dynamically regulated throughout the cell cycle stages, but it is still unclear whether the centrosomal residency of p150(glued) correlated with cell cycle progression. Here we found that p150(glued) was located in the mother centriole during G1/S stage and its centrosomal residency was independent of microtubule transportation. However, the centrosomal p150(glued) became blurred at G2/M phase and this event was not regulated by its phosphorylation. Entering into mitosis, p150(glued) was robustly enriched in the mitotic spindle nearby the spindle poles but not in the centrosome. During serum starvation (G0 stage), p150(glued) appeared at the base of primary cilium and its depletion attenuated starvation-induced primary cilium formation. We also checked its role in the maintenance of centrosome homeostasis and configuration, and found depletion of p150(glued) did not induce centrosome amplification or splitting but inhibited U2OS cell growth. G1 arrest and reduced EdU incorporation were observed in p150(glued) deficient U2OS cells. In addition, cyclin E was downregulated following p150(glued) depletion. The p53/p21 signaling was activated indicating that CDKs were inactivated. The reduced cell growth was ameliorated in the p150(glued) depleted cells when treated with p53 inhibitor. Thus, we have identified the centrosomal targeting of p150(glued) in distinct cell cycle stage and uncovered its role in controlling G1/S transition., (© 2015 Wiley Periodicals, Inc.)

Aim: To explore the bioactivity of an ethanolic extract of Schizandra arisanensis (SA-Et) and isolated constituents against interleukin-1β and interferon-γ-mediated β cell death and abolition of insulin secretion., Methods: By employing BRIN-BD11 cells, the effects of SA-Et administration on cytokine-mediated cell death and abolition of insulin secretion were evaluated by a viability assay, cell cycle analysis, and insulin assay. The associated gene and protein expressions were also measured. In addition, the bioactivities of several peak compounds collected from the SA-Et were tested against cytokine-mediated β cell death., Results: Our results revealed that SA-Et dose-dependently ameliorated cytokine-mediated β cell death and apoptosis. Instead of suppressing inducible nitric oxide synthase/nitric oxide cascade or p38MAPK activity, suppression of stress-activated protein kinase/c-Jun NH2-terminal kinase activity appeared to be the target for SA-Et against the cytokine mix. In addition, SA-Et provided some insulinotropic effects which re-activated the abolished insulin exocytosis in cytokine-treated BRIN-BD11 cells. Finally, schiarisanrin A and B isolated from the SA-Et showed a dose-dependent protective effect against cytokine-mediated β cell death., Conclusion: This is the first report on SA-Et ameliorating cytokine-mediated β cell death and dysfunction via anti-apoptotic and insulinotropic actions.

To describe epidemiologic characteristics of norovirus infection and its genotype in Shenzhen area of 2010. Stool specimens were collected from four monitoring point and detected by reverse transcription polymerase chain reaction (PT-PCR). Positive PCR products were purified and sequenced, and the sequences were performed by Clustal W and MEGA 4.0 programs, then genotype was identified and phylogenetic tree was constructed. Nucleotide sequence analysis revealed that 79 strains of NV belonged to norovirus genogroup II and 6 belonged to genogroup 1 of all 85 positive products. While 55 strains belonged to G II/4(2006b), 16 strains belonged to G II/4(2008 variant), 2 strains belonged to G II /1, 4 strains belonged to G II/5, 2 strains belonged to G II/11, 1 strain belonged to GII/4, 2 strains belonged to GII/5, 3 strains belonged to GI/6. The main genogroups of norovirus in Shenzhen ware GI and G II. G II /4 was one of the most major genotype of norovirus , while G II /4(2006b) variant was identified as the predominant strain in Shenzhen area.