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首页> 外文期刊>Current Genetics >The interaction of induction, repression and starvation in the regulation of extracellular proteases in Aspergillus nidulans: evidence for a role for CreA in the response to carbon starvation
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The interaction of induction, repression and starvation in the regulation of extracellular proteases in Aspergillus nidulans: evidence for a role for CreA in the response to carbon starvation

机译:构巢曲霉细胞外蛋白酶调控中诱导,抑制和饥饿的相互作用:CreA在碳饥饿响应中的作用证据

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摘要

In Aspergillus nidulans, production of extracellular proteases in response to carbon starvation and to a lesser extent nitrogen starvation is controlled by XprG, a putative transcriptional activator. In this study the role of genes involved in carbon catabolite repression and the role of protein as an inducer of extracellular protease gene expression were examined. The addition of exogenous protein to the growth medium did not increase extracellular protease activity whether or not additional carbon or nitrogen sources were present indicating that induction does not play a major role in the regulation of extracellular proteases. Northern blot analysis confirmed that protein is not an inducer of the major A. nidulans protease, PrtA. Mutations in the creA, creB and creC genes increased extracellular protease levels in medium lacking a carbon source suggesting that they may have a role in the response to carbon starvation as well as carbon catabolite repression. Analysis of glkA4 frA2 and creAΔ4 mutants showed that the loss of glucose signalling or the DNA-binding protein which mediates carbon catabolite repression did not abolish glucose repression but did increase extracellular protease activity. This increase was XprG-dependent indicating that the effect of these genes may be through modulation of XprG activity.
机译:在构巢曲霉中,响应于碳饥饿和较小程度的氮饥饿的胞外蛋白酶的产生受XprG(一种假定的转录激活因子)控制。在这项研究中,研究了参与碳分解代谢物阻遏的基因的作用以及蛋白质作为细胞外蛋白酶基因表达的诱导剂的作用。无论是否存在额外的碳源或氮源,向生长培养基中添加外源蛋白都不会增加细胞外蛋白酶的活性,这表明诱导作用在细胞外蛋白酶的调节中不起主要作用。 Northern印迹分析证实蛋白质不是主要构巢曲霉蛋白酶PrtA的诱导物。 creA,creB和creC基因中的突变会增加缺少碳源的培养基中的细胞外蛋白酶水平,这表明它们可能在对碳饥饿以及碳分解代谢物阻遏的反应中发挥作用。 glkA4 frA2和creAΔ4突变体的分析表明,葡萄糖信号传导或介导碳分解代谢物阻遏作用的DNA结合蛋白的丧失并没有消除葡萄糖阻遏作用,但确实增加了细胞外蛋白酶的活性。这种增加是XprG依赖性的,表明这些基因的作用可能是通过XprG活性的调节。

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