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构巢曲霉中细胞外蛋白酶调控过程中诱导、阻遏和饥饿的相互作用:CreA在碳饥饿应答中作用的证据

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.

作者信息

Katz Margaret E, Bernardo Stella M, Cheetham Brian F

机构信息

Molecular and Cellular Biology, University of New England, Armidale, NSW 2351, Australia.

出版信息

Curr Genet. 2008 Jul;54(1):47-55. doi: 10.1007/s00294-008-0198-6. Epub 2008 May 30.

Abstract

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 creADelta4 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.

摘要

在构巢曲霉中,响应碳饥饿以及在较小程度上响应氮饥饿时胞外蛋白酶的产生受XprG(一种假定的转录激活因子)控制。在本研究中,检测了参与碳分解代谢物阻遏的基因的作用以及蛋白质作为胞外蛋白酶基因表达诱导物的作用。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质均未增加胞外蛋白酶活性,这表明诱导在胞外蛋白酶的调控中不发挥主要作用。Northern印迹分析证实蛋白质不是构巢曲霉主要蛋白酶PrtA的诱导物。creA、creB和creC基因中的突变增加了缺乏碳源的培养基中的胞外蛋白酶水平,这表明它们可能在对碳饥饿以及碳分解代谢物阻遏的响应中发挥作用。对glkA4 frA2和creADelta4突变体的分析表明,葡萄糖信号传导的丧失或介导碳分解代谢物阻遏的DNA结合蛋白的缺失并未消除葡萄糖阻遏,但确实增加了胞外蛋白酶活性。这种增加依赖于XprG,表明这些基因的作用可能是通过调节XprG活性来实现的。

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