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Respiratory Growth (respiratory + growth)
Selected AbstractsThe response of the yeast Saccharomyces cerevisiae to sudden vs. gradual changes in environmental stress monitored by expression of the stress response protein Hsp12pFEMS YEAST RESEARCH, Issue 6 2008Ildar Nisamedtinov Abstract The response of the yeast Saccharomyces cerevisiae to sudden vs. gradual changes in different environmental stress conditions during both respiratory growth and aerobic fermentative growth in the presence of excess glucose was investigated by monitoring the level and rate of expression of the stress response protein Hsp12p using the fluorescent fusion construct Hsp12p-Gfp2p. The initial expression level and the rate of Hsp12p synthesis was significantly greater under glucose-limited conditions in the chemostat (D<0.14 h,1) compared with when excess glucose was present in the auxostat. Decreasing the dilution rate and the glucose concentration further in the A-stat resulted in increased Hsp12p expression, which was more marked when a rapid rather than a gradual change was affected. Common stress factors such as NaCl, ethanol and elevated temperature caused stress responses in both D-stat and auxo-accelerostat culture. The magnitude of the stress response depended on the stress factor, cultivation conditions as well as the rate of change of the stress factor. The rate of Hsp12p synthesis increased due to all applied stresses, with the observed increase between 2 and 20 times lower when the stress was applied gradually rather than rapidly. The results suggested that the Hsp12p expression rate is a good indicator of applied stress in S. cerevisiae. [source] The Kluyver effect revisitedFEMS YEAST RESEARCH, Issue 4 2003Hiroshi Fukuhara Abstract Yeast species can grow on various sugars. However, in many cases the growth on certain sugars (especially oligosaccharides) occurs only under aerobic conditions, and not in anaerobiosis or in the absence of respiration. Fermentation is blocked under these conditions. This apparent dependence of sugar utilization on the respiration has been called Kluyver effect, and such ,respiration-dependent' species are called Kluyver effect positive. A yeast may be Kluyver effect positive for some sugars and not for others. The physiological meaning and the molecular basis of the phenomenon are not clear. It has recently been reported that Kluyveromyces lactis, which is Kluyver effect positive for galactose and a few other sugars, could be converted into a Kluyver effect-negative form by introduction of relevant sugar transporter genes. Such results offer for the first time a direct support to the hypothesis that the immediate cause of the Kluyver effect may be the low level of sugar transporter activities which is not sufficient to sustain the high substrate flow necessary for fermentative growth, whereas the energy-efficient respiratory growth does not require a high rate of sugar uptake. We examined to what extent this sugar transporter theory of the Kluyver effect can be generalized. [source] Triclosan inhibition of mycobacterial InhA in Saccharomyces cerevisiae: yeast mitochondria as a novel platform for in vivo antimycolate assaysLETTERS IN APPLIED MICROBIOLOGY, Issue 4 2010A. Gurvitz Abstract Aims:, To demonstrate the suitability of yeast to act as a novel biotechnological platform for conducting in vivo inhibition assays using drugs with low efficacies towards their mycobacterial targets, such as occurs in the situation with triclosan and InhA. Methods and Results:, A surrogate yeast host represented by Saccharomyces cerevisiae etr1, cells lacking Etr1p, the 2- trans -enoyl-thioester reductase of mitochondrial type 2 fatty acid synthase (FASII), was designed to rely on the Mycobacterium tuberculosis FASII enzyme InhA. Although InhA is 10 000 times less sensitive to the antimicrobial drug triclosan than is bacterial FabI, the respiratory growth of yeast cells depending on InhA was severely affected on glycerol medium containing triclosan. Conclusions:, The yeast system could detect enzyme inhibition despite the use of a drug with only low efficacy. Significance and Impact of the Study:, Tuberculosis affects a third of the human population, and InhA is a major drug target for combating this disease. InhA is inhibited by isoniazid, but triclosan-derived compounds are presently being developed as antimycolates. A demonstration of triclosan inhibition of InhA in yeast represents a meaningful variation in studying this effect in mycobacteria, because it occurred without the potentially confusing aspects of perturbing protein,protein interactions which are presumed vital to mycobacterial FASII, inactivating other important enzymes or eliciting a dedicated transcriptional response in Myco. tuberculosis. [source] Overexpression of Upf1p compensates for mitochondrial splicing deficiency independently of its role in mRNA surveillanceMOLECULAR MICROBIOLOGY, Issue 4 2004B. De Pinto Summary In yeast the UPF1, UPF2 and UPF3 genes encode three interacting factors involved in translation termination and nonsense-mediated mRNA decay (NMD). UPF1 plays a central role in both processes. In addition, UPF1 was originally isolated as a multicopy suppressor of mitochondrial splicing deficiency, and its deletion leads to an impairment in respiratory growth. Here, we provide evidence that inactivation of UPF2 or ,UPF3, ,like ,that ,of ,UPF1, ,leads ,to ,an ,impairment in respiratory competence, suggesting that their products, Upf1p, Upf2p and Upf3p, are equivalently involved in mitochondrial biogenesis. In addition, however, we show that only Upf1p acts as a multicopy suppressor of mitochondrial splicing deficiency, and its activity does not require either Upf2p or Upf3p. Mutations in the conserved cysteine- and histidine-rich regions and ATPase and helicase motifs of Upf1p separate the ability of Upf1p to complement the respiratory impairment of a ,upf1 strain from its ability to act as a multicopy suppressor of mitochondrial splicing deficiency, indicating that distinct pathways express these phenotypes. In addition, we show that, when overexpressed, Upf1p is not detected within mitochondria, suggesting that its role as multicopy suppressor of mitochondrial splicing deficiency is indirect. Furthermore, we provide evidence that cells overexpressing certain upf1 alleles accumulate a phosphorylated isoform of Upf1p. Altogether, these results indicate that overexpression of Upf1p compensates for mitochondrial splicing deficiency independently of its role in mRNA surveillance, which relies on Upf1p,Upf2p,Upf3p functional interplay. [source] | ||||||||||