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991.
An insertional point mutation inactivates NolR repressor in Rhizobium meliloti 1021. 总被引:2,自引:1,他引:1 下载免费PDF全文
In the majority of Rhizobium meliloti isolates, nod gene expression is controlled by NolR, but this is not the case in a few strains including the widely used laboratory strain 1021. In 1021, the lack of NolR function was shown to be due to a single insertional mutation in the C-terminal coding sequence which abolished the DNA-binding ability, though the helix-turn-helix motif remained intact. This indicates that the C-terminal part of the protein is also essential for DNA binding. We conclude that in this species, control of nod gene expression involves NolR and strain 1021 represents an exception in which the NolR function was lost by a single event. 相似文献
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Observations were made on a well-habituated natural troop of Japanese macaques (Macaca fuscata yakui), living in warm-temperate, lowland forest in Yakushima. Between mid-May and the end of June the macaques feed on the fruit of the evergreen tree Myrica rubra (Myricaceae). The fruit of this species are abundant in some years and scarce in others. Data were compared for two heavy-fruiting years (1988 and 1990) and one poor-fruiting year (1991) to examine the influence of fruit availability on patterns of foraging, ranging, and the frequency of inter-troop encounters. In both heavy-fruiting years M. rubra fruit accounted for a maximum of over 70% of foraging time, compared with a maximum of <5% in the poor-fruiting year. Heavy fruiting was also associated with a marked decrease in the overall time spent foraging. In early May of all three years troop movements were largely confined to northern parts of the home range. By early June of both heavy-fruiting years ranging had shifted to the south-west, and included an area with a high concentration of M. rubra trees. This area was rarely visited at other times, and was not visited during the study period in the poor-fruiting year. The overlap in range-use between the two heavy-fruiting years was significantly greater than that between the heavy-fruiting years and the poor-fruiting year. Heavy fruiting was also associated with an increase in the frequency of inter-troop encounters. © 1995 Wiley-Liss, Inc. 相似文献
998.
A Gram-positive Rhodococcus erythropolis strain S1 was shown to assimilate aromatic amino acids such as L-phenylalanine, L-tyrosine, L-tryptophan, D-phenylalanine, D-tyrosine and D-tryptophan, which were utilized not only as the sole carbon source but also as a suitable nitrogen source. The highest growth on these aromatic amino acids occurred at a temperature of 30°C. L-Phenylalanine, L-tyrosine and L-tryptophan degradative pathways would appear to be independent, and to be induced alternatively. The strain S1 also showed the ability to assimilate peptides which consisted of only L-phenylalanine and L-tyrosine. 相似文献
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Miranda Kleijn Harry O. Voorma Adri A. M. Thomas 《Journal of cellular biochemistry》1995,59(4):443-452
Mitogenic stimulation of protein synthesis is accompanied by an increase in elF-4E phosphorylation. The effect on protein synthesis by induction of differentiation is less well known. We treated P19 embryonal carcinoma cells with the differentiating agent retinoic acid and found that protein synthesis increased during the first hour of addition. However, the phosphorylation state, as well as the turnover of phosphate on elF-4E, remained unchanged. Apparently, the change in protein synthesis after RA addition is regulated by another mechanism than elF-4E phosphorylation. By using P19 cells overexpressing the EGF receptor, we show that the signal transduction pathway that leads to phosphorylation of elF-4E is present in P19 cells; the EGF-induced change in phosphorylation of elF-4E in these cells is likely to be regulated by a change in elF-4E phosphatase activity. These results suggest that the onset of retinoic acid-induced differentiation is triggered by a signal transduction pathway which involves changes in protein synthesis, but not elF-4E phosphorylation. © 1995 Wiley-Liss, Inc. 相似文献