Identification and characterization of a fluorescent flagellar protein from the brown alga Scytosiphon lomentaria (Scytosiphonales, Phaeophyceae): A flavoprotein homologous to Old Yellow Enzyme

The posterior flagellum of the zoospore of the brown alga Scytosiphon lomentaria exhibits bright green autofluorescence. To identify the fluorescent flagellar substance(s), we isolated flagella from zoospores and partially purified a flavoprotein by anion-exchange and gel-filtration chromatography. Spectrofluorometric and chromatographic analyses showed that the flavoprotein had an apparent molecular mass of 41 kDa and a non-covalently bound flavin mononucleotide as a chromophore. Based on partial amino acid sequences of the protein, a cDNA of the 41-kDa flavoprotein was cloned and sequenced. The deduced amino acid sequence of the cDNA was homologous to that of the Old Yellow Enzyme family distributed in proteobacteria, yeasts and vascular plants

Marylosides A-G, Norcycloartane Glycosides from Leaves of Cymbidium Great Flower ‘Marylaurencin’

Seven novel norcycloartane glycosides, maryloside A–G (1–7), were isolated from the leaves of Cymbidium Great Flower ‘Marylaurencin’, along with a known norcycloartane glycoside, cymbidoside (8). These structures were determined on the basis of mainly NMR experiments as well as chemical degradation and X-ray crystallographic analysis. The isolated compounds (1–6 and 8) were evaluated for the inhibitory activity on lipopolysaccharide (LPS) and interferon-γ (IFN-γ)-stimulated nitric oxide (NO) production in RAW 264.7 cells. Consequently, 1 and 3 exhibited moderate activity

Genotoxic Stress Abrogates Renewal of Melanocyte Stem Cells by Triggering Their Differentiation

SummarySomatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a “stemness checkpoint” to maintain the stem cell quality and quantity

Functional expression of carnitine/organic cation transporter OCTN1 in mouse brain neurons: Possible involvement in neuronal differentiation

The aim of the present study is to clarify the functional expression and physiological role in brain neurons of carnitine/organic cation transporter OCTN1/SLC22A4, which accepts the naturally occurring antioxidant ergothioneine (ERGO) as a substrate in vivo. After intracerebroventricular administration, the distribution of [ 3H]ERGO in several brain regions of octn1 -/- mice was much lower than that in wild-type mice, whereas extracellular marker [ 14C]mannitol exhibited similar distribution in the two strains. The [ 3H]ERGO distribution in wild-type mice was well correlated with the amount of ERGO derived from food intake and the OCTN1 mRNA level in each brain region. Immunohistochemical analysis revealed colocalization of OCTN1 with neuronal cell markers microtubule-associated protein 2 (MAP2) and βIII-tubulin in mouse brain and primary cultured cortical neurons, respectively. Moreover, cultured cortical neurons exhibited time-dependent and saturable uptake of [ 3H]ERGO. These results demonstrate that OCTN1 is functionally expressed in brain neurons. The addition of ERGO simultaneously with serum to culture medium of cortical neurons attenuated mRNA and protein expressions of MAP2, βIII-tubulin and synapse formation marker synapsin I, and induced those of sex determining region Y-box 2 (Sox2), which is required to maintain the properties of undifferentiated neural stem cells. In neuronal model Neuro2a cells, knockdown of OCTN1 by siRNA reduced the uptake of [ 3H]ERGO with concomitant up-regulation of oxidative stress marker HO-1 and Sox2, and down-regulation of neurite outgrowth marker GAP43. Interestingly, the siRNA knockdown decreased the number of differentiated Neuro2a cells showing long neurites, but increased the total number of cells. Thus, OCTN1 is involved in cellular differentiation, but inhibits their proliferation, possibly via the regulation of cellular oxidative stress. This is the first evidence that OCTN1 plays a role in neuronal differentiation and proliferation, which are required for brain development. Crown Copyright © 2012

Real-time In Situ Electron Spin Resonance Measurements on Fungal Spores of Penicillium digitatum during Exposure of Oxygen Plasmas

We report the kinetic analysis of free radicals on fungal spores of Penicillium digitatum interacted with atomic oxygen generated plasma electric discharge using real time in situ electron spin resonance (ESR) measurements. We have obtained information that the ESR signal from the spores was observed and preliminarily assignable to semiquinone radical with a g-value of around 2.004 and a line width of approximately 5G. The decay of the signal is possibly linked to the inactivation of the fungal spore. The real-time in situ ESR has proven to be a useful method to elucidate plasma-induced surface reactions on biological specimens.Comment: 11 pages, 5 figure

Molecular Characterization of Cryptosporidium Isolates Obtained from Human and Bovine Infections in Japan

Cryptosporidiumポリスレオニン遺伝子のPCR/RFLP分析により、わが国で分離されたヒト由来Cryptosporidium22株は、ヒト型C.parvum(genotype1)、動物型C.parvum(genotype2)、トリ型C.meleagridis(genotype3)の3遺伝子型に明瞭に型別された。ヒト由来genotype3のC.meleagridis分離株は、Cryptosporidium18S　rRNA遺伝子のシークエンス分析により同定され、その存在が本邦で初めて確認された

Genotoxic stress abrogates renewal of melanocyte stem cells by triggering their differentiation.

金沢大学医薬保健研究域　医学系Somatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a "stemness checkpoint" to maintain the stem cell quality and quantity. © 2009 Elsevier Inc. All rights reserved