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121.
Loss of cell wall alpha(1-3) glucan affects Cryptococcus neoformans from ultrastructure to virulence 总被引:1,自引:0,他引:1
Reese AJ Yoneda A Breger JA Beauvais A Liu H Griffith CL Bose I Kim MJ Skau C Yang S Sefko JA Osumi M Latge JP Mylonakis E Doering TL 《Molecular microbiology》2007,63(5):1385-1398
Yeast cell walls are critical for maintaining cell integrity, particularly in the face of challenges such as growth in mammalian hosts. The pathogenic fungus Cryptococcus neoformans additionally anchors its polysaccharide capsule to the cell surface via alpha(1-3) glucan in the wall. Cryptococcal cells disrupted in their alpha glucan synthase gene were sensitive to stresses, including temperature, and showed difficulty dividing. These cells lacked surface capsule, although they continued to shed capsule material into the environment. Electron microscopy showed that the alpha glucan that is usually localized to the outer portion of the cell wall was absent, the outer region of the wall was highly disorganized, and the inner region was hypertrophic. Analysis of cell wall composition demonstrated complete loss of alpha glucan accompanied by a compensatory increase in chitin/chitosan and a redistribution of beta glucan between cell wall fractions. The mutants were unable to grow ina mouse model of infection, but caused death in nematodes. These studies integrate morphological and biochemical investigations of the role of alpha glucan in the cryptococcal cell wall. 相似文献
122.
Hirokawa YS Takagi A Uchida K Kozuka Y Yoneda M Watanabe M Shiraishi T 《Cellular & molecular biology letters》2007,12(3):370-377
In this paper, we describe the isolation and characterization of two PC3 subclones. One subclone, mr, showed an epithelial
phenotype, the other, M1, showed a sarcomatous morphology. Transplanted into nude mice, mr developed tumors at a dramatically
faster rate than M1. Comparing the two subclones, differentially expressed genes were identified, including E-cadherin, IL-8
and STAG1/PMEPA1. These genes were expressed at higher levels in mr than in M1. 相似文献
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Sho Aki Kazuaki Yoshioka Yasuo Okamoto Noriko Takuwa Yoh Takuwa 《The Journal of biological chemistry》2015,290(10):6086-6105
We have recently demonstrated that the PI3K class II-α isoform (PI3K-C2α), which generates phosphatidylinositol 3-phosphate and phosphatidylinositol 3,4-bisphosphates, plays crucial roles in angiogenesis, by analyzing PI3K-C2α knock-out mice. The PI3K-C2α actions are mediated at least in part through its participation in the internalization of VEGF receptor-2 and sphingosine-1-phosphate receptor S1P1 and thereby their signaling on endosomes. TGFβ, which is also an essential angiogenic factor, signals via the serine/threonine kinase receptor complex to induce phosphorylation of Smad2 and Smad3 (Smad2/3). SARA (Smad anchor for receptor activation) protein, which is localized in early endosomes through its FYVE domain, is required for Smad2/3 signaling. In the present study, we showed that PI3K-C2α knockdown nearly completely abolished TGFβ1-induced phosphorylation and nuclear translocation of Smad2/3 in vascular endothelial cells (ECs). PI3K-C2α was necessary for TGFβ-induced increase in phosphatidylinositol 3,4-bisphosphates in the plasma membrane and TGFβ receptor internalization into the SARA-containing early endosomes, but not for phosphatidylinositol 3-phosphate enrichment or localization of SARA in the early endosomes. PI3K-C2α was also required for TGFβ receptor-mediated formation of SARA-Smad2/3 complex. Inhibition of dynamin, which is required for the clathrin-dependent receptor endocytosis, suppressed both TGFβ receptor internalization and Smad2/3 phosphorylation. TGFβ1 stimulated Smad-dependent VEGF-A expression, VEGF receptor-mediated EC migration, and capillary-like tube formation, which were all abolished by either PI3K-C2α knockdown or a dynamin inhibitor. Finally, TGFβ1-induced microvessel formation in Matrigel plugs was greatly attenuated in EC-specific PI3K-C2α-deleted mice. These observations indicate that PI3K-C2α plays the pivotal role in TGFβ receptor endocytosis and thereby Smad2/3 signaling, participating in angiogenic actions of TGFβ. 相似文献
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Fukada S Yamaguchi M Kokubo H Ogawa R Uezumi A Yoneda T Matev MM Motohashi N Ito T Zolkiewska A Johnson RL Saga Y Miyagoe-Suzuki Y Tsujikawa K Takeda S Yamamoto H 《Development (Cambridge, England)》2011,138(21):4609-4619
Satellite cells, which are skeletal muscle stem cells, divide to provide new myonuclei to growing muscle fibers during postnatal development, and then are maintained in an undifferentiated quiescent state in adult skeletal muscle. This state is considered to be essential for the maintenance of satellite cells, but their molecular regulation is unknown. We show that Hesr1 (Hey1) and Hesr3 (Heyl) (which are known Notch target genes) are expressed simultaneously in skeletal muscle only in satellite cells. In Hesr1 and Hesr3 single-knockout mice, no obvious abnormalities of satellite cells or muscle regenerative potentials are observed. However, the generation of undifferentiated quiescent satellite cells is impaired during postnatal development in Hesr1/3 double-knockout mice. As a result, myogenic (MyoD and myogenin) and proliferative (Ki67) proteins are expressed in adult satellite cells. Consistent with the in vivo results, Hesr1/3-null myoblasts generate very few Pax7(+) MyoD(-) undifferentiated cells in vitro. Furthermore, the satellite cell number gradually decreases in Hesr1/3 double-knockout mice even after it has stabilized in control mice, and an age-dependent regeneration defect is observed. In vivo results suggest that premature differentiation, but not cell death, is the reason for the reduced number of satellite cells in Hesr1/3 double-knockout mice. These results indicate that Hesr1 and Hesr3 are essential for the generation of adult satellite cells and for the maintenance of skeletal muscle homeostasis. 相似文献
129.
Enhancing bioremediation of diesel-fuel-contaminated soil in a boreal climate: Comparison of biostimulation and bioaugmentation 总被引:2,自引:0,他引:2
Sari Kauppi Aki Sinkkonen Martin Romantschuk 《International biodeterioration & biodegradation》2011,65(2):359-368
Cold conditions delay bioremediation of oil hydrocarbons, but other bottlenecks also affect the outcome. Means to stimulate biodegradation of diesel oil hydrocarbons in contaminated soil were compared. Different combinations of nutrients, bulking agent, aeration, and microbial inocula were examined in lab simulations, and effective combinations were tested in field conditions. Bacterial communities were investigated by cloning and sequencing 16S-rRNA genes. Efficient degradation was attained when slow-release nutrients and aeration were used simultaneously. Bacterial inocula did not advance soil remediation, nor did they have any lasting effect on bacterial densities. Bacteria belonging to Proteobacteria were dominant in all cases. In the field test, a bulking agent promoting air passage through the soil ensured sufficient aeration, while forced air decreased the soil moisture excessively. We concluded that biostimulation via optimization of nitrogen and oxygen supply significantly improved bioremediation of oil-contaminated soil, while bioaugmentation had no additional effect. 相似文献
130.
Pamela K Wagner Aki Otomo Julian K Christians 《Reproductive biology and endocrinology : RB&E》2011,9(1):48