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41.
42.
Summary The Bangia and Conchocelis-phases of Bangia fuscopurpurea were studied light and electron microscopically. Typical florideophycean algal pit connections were found in the Conchocelis-phase and were lacking in the Bangia-phase. Electron microscopy has revealed that these dumbell-shaped structures are membrane bound plugs continuous between adjacent cells. The presence of such entities in one stage of the life cycle of a bangiophycean alga, once thought to be unique to the higher red algal subclass Florideophycidae, indicates closer evolutionary ties between the two subclasses. 相似文献
43.
44.
Alexander A. Shestov Anthony Mancuso Seung-Cheol Lee Lili Guo David S. Nelson Jeffrey C. Roman Pierre-Gilles Henry Dennis B. Leeper Ian A. Blair Jerry D. Glickson 《The Journal of biological chemistry》2016,291(10):5157-5171
A network model for the determination of tumor metabolic fluxes from 13C NMR kinetic isotopomer data has been developed and validated with perfused human DB-1 melanoma cells carrying the BRAF V600E mutation, which promotes oxidative metabolism. The model generated in the bonded cumomer formalism describes key pathways of tumor intermediary metabolism and yields dynamic curves for positional isotopic enrichment and spin-spin multiplets. Cells attached to microcarrier beads were perfused with 26 mm [1,6-13C2]glucose under normoxic conditions at 37 °C and monitored by 13C NMR spectroscopy. Excellent agreement between model-predicted and experimentally measured values of the rates of oxygen and glucose consumption, lactate production, and glutamate pool size validated the model. ATP production by glycolytic and oxidative metabolism were compared under hyperglycemic normoxic conditions; 51% of the energy came from oxidative phosphorylation and 49% came from glycolysis. Even though the rate of glutamine uptake was ∼50% of the tricarboxylic acid cycle flux, the rate of ATP production from glutamine was essentially zero (no glutaminolysis). De novo fatty acid production was ∼6% of the tricarboxylic acid cycle flux. The oxidative pentose phosphate pathway flux was 3.6% of glycolysis, and three non-oxidative pentose phosphate pathway exchange fluxes were calculated. Mass spectrometry was then used to compare fluxes through various pathways under hyperglycemic (26 mm) and euglycemic (5 mm) conditions. Under euglycemic conditions glutamine uptake doubled, but ATP production from glutamine did not significantly change. A new parameter measuring the Warburg effect (the ratio of lactate production flux to pyruvate influx through the mitochondrial pyruvate carrier) was calculated to be 21, close to upper limit of oxidative metabolism. 相似文献
45.
The role of alcohol dehydrogenase (ADH) activity in ethanol toxicity was investigated in Drosophila melanogaster. Flies from three congenic Adh strains (high, medium, and low ADH activity) were allowed to deposit eggs on medium containing 0, 4, or 8% ethanol. The resulting larvae were allowed to complete their development in the medium, and emerging flies were examined for defects. Flies with high ADH activity had malformation incidences of 0.8, 2.4, and 5.2% at 0, 4, and 8% ethanol, respectively. The comparable incidences for the low ADH strain were 1.0, 4.1, and 8.4%, while those for the medium ADH strain were intermediate in value. These results indicate that ethanol teratogenesis may be inversely related to ADH activity. When larvae were treated with ethanol for different lengths of time during development, the incidence of defects in flies from the high ADH strain was 3.9% when exposure started at the first instar and 3.09% when exposure started at the third instar. Results of the same exposures for the intermediate ADH strain were 5.2 and 3.4%, respectively, while those for the low ADH strain were 6.9 and 5.5%, respectively. Thus, length of ethanol exposure was directly related to the increased incidence of malformations in all tested Drosophila strains. For all tested strains, defect incidences appeared to be dose-related as well, regardless of length of exposure. ADH in Drosophila has a dual function and thus can catalyze oxidation of both ethanol and its toxic metabolite, acetaldehyde. This suggests that ethanol is the proximate teratogen in Drosophila. 相似文献
46.
Goldstein DB; Zhivotovsky LA; Nayar K; Linares AR; Cavalli-Sforza LL; Feldman MW 《Molecular biology and evolution》1996,13(9):1213-1218
It has recently been suggested that observed levels of variation at
microsatellite loci can be used to infer patterns of selection in genomes
and to assess demographic history. In order to evaluate the feasibility of
these suggestions it is necessary to know something about how levels of
variation at microsatellite loci are expected to fluctuate due simply to
stochasticity in the processes of mutation and inheritance (genetic
sampling). Here we use recently derived properties of the stepwise mutation
model to place confidence intervals around the variance in repeat score
that is expected at mutation-drift equilibrium and outline a statistical
test for whether an observed value differs significantly from expectation.
We also develop confidence intervals for the time course of the buildup of
variation following a complete elimination of variation, such as might be
caused by a selective sweep or an extreme population bottleneck. We apply
these methods to the variation observed at human Y-specific
microsatellites. Although a number of authors have suggested the
possibility of a very recent sweep, our analyses suggest that a sweep or
extreme bottleneck is unlikely to have occurred anytime during the last
approximately 74,000 years. To generate this result we use a recently
estimated mutation rate for microsatellite loci of 5.6 x 10(-4) along with
the variation observed at autosomal microsatellite loci to estimate the
human effective population size. This estimate is 18,000, implying an
effective number of 4,500 Y chromosomes. One important general conclusion
to emerge from this study is that in order to reject mutation-drift
equilibrium at a set of linked microsatellite loci it is necessary to have
an unreasonably large number of loci unless the observed variance is far
below that expected at mutation-drift equilibrium.
相似文献
47.
48.
Effect of caffeine on radiation-induced mitotic delay: delayed expression of G2 arrest 总被引:1,自引:0,他引:1
In the presence of 5 mM caffeine, irradiated (1.5 Gy) S and G2 cells progressed to mitosis in register and without arrest in G2. Caffeine (5 mM) markedly reduced mitotic delay even after radiation doses up to 20 Gy. When caffeine was removed from irradiated (1.5 Gy) and caffeine-treated cells, a period of G2 arrest followed, similar in length to that produced by radiation alone. The arrest expressed was independent of the duration of the caffeine treatment for exposures up to 3 hr. The similarity of the response to the cited effects of caffeine on S-phase delay suggests a common basis for delay induction in S and G2 phases. 相似文献
49.
Role of RacC for the regulation of WASP and phosphatidylinositol 3-kinase during chemotaxis of Dictyostelium 总被引:1,自引:0,他引:1
WASP family proteins are key players for connecting multiple signaling pathways to F-actin polymerization. To dissect the highly integrated signaling pathways controlling WASP activity, we identified a Rac protein that binds to the GTPase binding domain of WASP. Using two-hybrid and FRET-based functional assays, we identified RacC as a major regulator of WASP. RacC stimulates F-actin assembly in cell-free systems in a WASP-dependent manner. A FRET-based microscopy approach showed local activation of RacC at the leading edge of chemotaxing cells. Cells overexpressing RacC exhibit a significant increase in the level of F-actin polymerization upon cAMP stimulation, which can be blocked by a phosphatidylinositol (PI) 3-kinase inhibitor. Membrane translocation of PI 3-kinase and PI 3,4,5-trisphosphate reporter is absent in racC null cells. Cells overexpressing dominant negative RacC mutants and racC null cells move at a significantly slower speed and show a poor directionality during chemotaxis. Our results suggest that RacC plays an important role in PI 3-kinase activation and WASP activation for dynamic regulation of F-actin assembly during Dictyostelium chemotaxis. 相似文献
50.
Nicholas J. Leeper Azad Raiesdana Yoko Kojima Hyung J. Chun Junya Azuma Lars Maegdefessel Ramendra K. Kundu Thomas Quertermous Philip S. Tsao Joshua M. Spin 《Journal of cellular physiology》2011,226(4):1035-1043
Aberrant smooth muscle cell (SMC) plasticity has been implicated in a variety of vascular disorders including atherosclerosis, restenosis, and abdominal aortic aneurysm (AAA) formation. While the pathways governing this process remain unclear, epigenetic regulation by specific microRNAs (miRNAs) has been demonstrated in SMCs. We hypothesized that additional miRNAs might play an important role in determining vascular SMC phenotype. Microarray analysis of miRNAs was performed on human aortic SMCs undergoing phenotypic switching in response to serum withdrawal, and identified 31 significantly regulated entities. We chose the highly conserved candidate miRNA‐26a for additional studies. Inhibition of miRNA‐26a accelerated SMC differentiation, and also promoted apoptosis, while inhibiting proliferation and migration. Overexpression of miRNA‐26a blunted differentiation. As a potential mechanism, we investigated whether miRNA‐26a influences TGF‐β‐pathway signaling. Dual‐luciferase reporter assays demonstrated enhanced SMAD signaling with miRNA‐26a inhibition, and the opposite effect with miRNA‐26a overexpression in transfected human cells. Furthermore, inhibition of miRNA‐26a increased gene expression of SMAD‐1 and SMAD‐4, while overexpression inhibited SMAD‐1. MicroRNA‐26a was also found to be downregulated in two mouse models of AAA formation (2.5‐ to 3.8‐fold decrease, P < 0.02) in which enhanced switching from contractile to synthetic phenotype occurs. In summary, miRNA‐26a promotes vascular SMC proliferation while inhibiting cellular differentiation and apoptosis, and alters TGF‐β pathway signaling. MicroRNA‐26a represents an important new regulator of SMC biology and a potential therapeutic target in AAA disease. J. Cell. Physiol. 226: 1035–1043, 2011. © 2010 Wiley‐Liss, Inc. 相似文献