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Increased Chitin Synthesis in Response to Type II Myosin Deficiency in Saccharomyces cerevisiae

机译:增加的几丁质酵母响应II型肌球蛋白缺乏几丁质的合成。

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We reported previously that the chitin content in cell walls of type II myosin-deficient Saccharomyces cerevisiae strains is increased relative to wile-type cells suggesting that increased chitin synthesis is induced in these strains.In the present study,we have performed enzyme activity assays for chitin synthases 1,2 and 3 to determine the exzyme isoform(s) involved.To determine if transcriptional regulation is involved,we conducted quantitative mRNA assays of the corresponding chitin synthase genes.We show that the enzyme activities of all three chitin synthases increase substantially over the wild-type strain while eight- and twofold increases in the mRNA levels for chitin synthases 1 and 3 were detected.Increases in enzyme activities and mRNA levels were not proportional.We conclude that the enzyme activities for all three chitin synthases are elevatedf in this strain and that this increase is mediated mainly by a posttranslational mechanism(s).The heightened sensitivity to osmotic stress and the corresponding increase in cell wall chitin contenat reported in these strains are consistent with a compensatory "stress response" mechanism induced by abnormal cell wall assembly.
机译:我们以前曾报道,II型肌球蛋白缺陷型酿酒酵母菌株的细胞壁中的几丁质含量相对于Wile型细胞有所增加,这表明这些菌株诱导了几丁质合成的增加。在本研究中,我们进行了酶活性测定几丁质合酶1,2和3来确定所涉及的酶同工型。为确定转录调控是否参与,我们对相应的几丁质合酶基因进行了定量mRNA检测。我们发现所有三种甲壳质合酶的酶活性均显着增加与野生型相比,几丁质合酶1和3的mRNA水平分别增加了8倍和2倍。酶活性和mRNA水平的增加不成比例。这种张力以及这种增加主要是由翻译后机制介导的。对渗透压的敏感性增强在这些菌株中报道的应激和细胞壁几丁质竞争性的相应增加与异常细胞壁装配诱导的补偿性“应激反应”机制一致。

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