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1.
Genetic tailoring of N-linked oligosaccharides: the role of glucose residues in glycoprotein processing of Saccharomyces cerevisiae in vivo 总被引:1,自引:0,他引:1
In higher eukaryotes a quality control system monitoring the folding state
of glycoproteins is located in the ER and is composed of the proteins
calnexin, calreticulin, glucosidase II, and UDP-glucose: glycoprotein
glucosyltransferase. It is believed that the innermost glucose residue of
the N- linked oligosaccharide of a glycoprotein serves as a tag in this
control system and therefore performs an important function in the protein
folding pathway. To address this function, we constructed Saccharomyces
cerevisiae strains which contain nonglucosylated (G0), monoglucosylated
(G1), or diglucosylated (G2) glycoproteins in the ER and used these strains
to study the role of glucose residues in the ER processing of
glycoproteins. These alterations of the oligosaccharide structure did not
result in a growth phenotype, but the induction of the unfolded protein
response upon treatment with DTT was much higher in G0 and G2 strains as
compared to wild-type and G1 strains. Our results provide in vivo evidence
that the G1 oligosaccharide is an active oligosaccharide structure in the
ER glycoprotein processing pathway of S.cerevisiae. Furthermore, by
analyzing N- linked oligosaccharides of the constructed strains we can
directly show that no general glycoprotein glucosyltransferase exists in S.
cerevisiae.
相似文献
2.
Gabriel Kyle T. Neville John J. Pierce George E. Cornelison Christopher T. 《Mycopathologia》2019,184(5):625-636
Mycopathologia - Pseudogymnoascus destructans is the causative agent of a fungal infection of bats known as white-nose syndrome (WNS). Since its discovery in 2006, it has been responsible for... 相似文献
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MyoD(-/-) satellite cells in single-fiber culture are differentiation defective and MRF4 deficient 总被引:9,自引:0,他引:9
MyoD-deficient mice are without obvious deleterious muscle phenotype during embryogenesis and fetal development, and adults in the laboratory have grossly normal skeletal muscle and life span. However, a previous study showed that in the context of muscle degeneration on a mdx (dystrophin null) genetic background, animals lacking MyoD have a greatly intensified disease phenotype leading to lethality not otherwise seen in mdx mice. Here we have examined MyoD(-/-) adult muscle fibers and their associated satellite cells in single myofiber cultures and describe major phenotypic differences found at the tissue, cellular, and molecular levels. The steady-state number of satellite cells on freshly isolated MyoD(-/-) fibers was elevated and abnormal branched fiber morphologies were observed, the latter suggesting chronic muscle regeneration in vivo. Single-cell RNA coexpression analyses were performed for c-met, m-cadherin, and the four myogenic regulatory factors (MRFs.) Most mutant satellite cells entered the cell cycle and upregulated expression of myf5, both characteristic early steps in satellite cell maturation. However, they later failed to normally upregulate MRF4, displayed a major deficit in m-cadherin expression, and showed a significant diminution in myogenin-positive status compared with wildtype. MyoD(-/-) satellite cells formed unusual aggregate structures, failed to fuse efficiently, and showed greater than 90% reduction in differentiation efficiency relative to wildtype. A further survey of RNAs encoding regulators of growth and differentiation, cell cycle progression, and cell signaling revealed similar or identical expression profiles for most genes as well as several noteworthy differences. Among these, GDF8 and Msx1 were identified as potentially important regulators of the quiescent state whose expression profile differs between mutant and wildtype. Considered together, these data suggest that activated MyoD(-/-) satellite cells assume a phenotype that resembles in some ways a developmentally "stalled" cell compared to wildtype. However, the MyoD(-/-) cells are not merely developmentally immature, as they also display novel molecular and cellular characteristics that differ from any observed in wild-type muscle precursor counterparts of any stage. 相似文献
5.
CA Kalva-Filho EZ Campos VL Andrade ASR Silva AM Zagatto MCS Lima M Papoti 《Biology of sport / Institute of Sport》2015,32(4):333-337
The aims of the present study were to investigate the relationship of aerobic and anaerobic parameters with 400 m performance, and establish which variable better explains long distance performance in swimming. Twenty-two swimmers (19.1±1.5 years, height 173.9±10.0 cm, body mass 71.2±10.2 kg; 76.6±5.3% of 400 m world record) underwent a lactate minimum test to determine lactate minimum speed (LMS) (i.e., aerobic capacity index). Moreover, the swimmers performed a 400 m maximal effort to determine mean speed (S400m), peak oxygen uptake () and total anaerobic contribution (CANA). The CANA was assumed as the sum of alactic and lactic contributions. Physiological parameters of 400 m were determined using the backward extrapolation technique ( and alactic contributions of CANA) and blood lactate concentration analysis (lactic anaerobic contributions of CANA). The Pearson correlation test and backward multiple regression analysis were used to verify the possible correlations between the physiological indices (predictor factors) and S400m (independent variable) (p < 0.05). Values are presented as mean ± standard deviation. Significant correlations were observed between S400m (1.4±0.1 m·s-1) and LMS (1.3±0.1 m·s-1; r = 0.80), (4.5±3.9 L·min-1; r = 0.72) and CANA (4.7±1.5 L·O2; r= 0.44). The best model constructed using multiple regression analysis demonstrated that LMS and explained 85% of the 400 m performance variance. When backward multiple regression analysis was performed, CANA lost significance. Thus, the results demonstrated that both aerobic parameters (capacity and power) can be used to predict 400 m swimming performance. 相似文献
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Polyana C Tizioto Jeremy F Taylor Jared E Decker Caio F Gromboni Mauricio A Mudadu Robert D Schnabel Luiz L Coutinho Gerson B Mour?o Priscila SN Oliveira Marcela M Souza James M Reecy Renata T Nassu Flavia A Bressani Patricia Tholon Tad S Sonstegard Mauricio M Alencar Rymer R Tullio Ana RA Nogueira Luciana CA Regitano 《遗传、选种与进化》2015,47(1)
7.
During development and regeneration, directed migration of cells, including neural crest cells, endothelial cells, axonal growth cones and many types of adult stem cells, to specific areas distant from their origin is necessary for their function. We have recently shown that adult skeletal muscle stem cells (satellite cells), once activated by isolation or injury, are a highly motile population with the potential to respond to multiple guidance cues, based on their expression of classical guidance receptors. We show here that, in vivo, differentiated and regenerating myofibers dynamically express a subset of ephrin guidance ligands, as well as Eph receptors. This expression has previously only been examined in the context of muscle-nerve interactions; however, we propose that it might also play a role in satellite cell-mediated muscle repair. Therefore, we investigated whether Eph-ephrin signaling would produce changes in satellite cell directional motility. Using a classical ephrin 'stripe' assay, we found that satellite cells respond to a subset of ephrins with repulsive behavior in vitro; patterning of differentiating myotubes is also parallel to ephrin stripes. This behavior can be replicated in a heterologous in vivo system, the hindbrain of the developing quail, in which neural crest cells are directed in streams to the branchial arches and to the forelimb of the developing quail, where presumptive limb myoblasts emigrate from the somite. We hypothesize that guidance signaling might impact multiple steps in muscle regeneration, including escape from the niche, directed migration to sites of injury, cell-cell interactions among satellite cell progeny, and differentiation and patterning of regenerated muscle. 相似文献
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