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Nuclear Accumulation of the GATA Factor AreA in Response to Complete Nitrogen Starvation by Regulation of Nuclear Export

机译:GATA因子AreA的核积累,响应于核出口监管对完全氮饥饿的反应

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Both the availability and the quality of nutrients affect cellular functions by controlling gene activity. AreA, a member of the GATA family of transcription factors, globally activates expression of genes involved in nitrogen source utilization in Aspergillus nidulans. The quality of the nitrogen source determines the level and activation capacity of AreA through controls at the level of areA mRNA stability and by interaction of AreA with the corepressor NmrA. The availability of potential nitrogen sources also affects the activation capacity of AreA. We show that the complete absence of a nitrogen source results in an enhanced level of AreA-dependent gene expression and that this response is independent of mechanisms regulating AreA activity in response to nitrogen source quality. During nitrogen starvation AreA accumulates in the nucleus, but the presence of a potential nitrogen source or carbon starvation prevents this accumulation. Furthermore, accumulated AreA is rapidly lost from the nuclei of nitrogen-starved cells when a nitrogen source is supplied or when a carbon source is absent, and this accompanies arrest of the AreA-dependent nitrogen starvation response on regulated gene expression. By the generation of a leptomycin B-sensitive mutant, we have been able to show that nuclear exit occurs via the CrmA exportin. We conclude that sensing mechanisms discriminate between starvation and the presence of potential nutrients that can signal to the AreA transcription factor. Nitrogen source availability, but not quality, affects nuclear accumulation by regulating nuclear exit of AreA, providing a rapid response to changes in the supply of nutrients.
机译:营养素的可用性和质量都会通过控制基因活性来影响细胞功能。 AreA是GATA转录因子家族的成员,在全球范围内激活构巢曲霉中氮源利用基因的表达。氮源的质量决定了AreA的水平和激活能力,它通过控制areA mRNA的稳定水平以及AreA与共抑制因子NmrA的相互作用。潜在氮源的可用性也影响AreA的激活能力。我们表明,完全不存在氮源会导致AreA依赖性基因表达水平提高,并且该响应独立于调节AreA活性以响应氮源质量的机制。在氮饥饿期间,AreA积累在原子核中,但是潜在氮源或碳饥饿的存在阻止了这种积累。此外,当提供氮源或缺少碳源时,累积的AreA会迅速从缺氮的细胞核中丢失,这伴随着AreA依赖型氮饥饿对调节基因表达的抑制作用。通过生成对Leptomycin B敏感的突变体,我们已经能够证明核出口是通过CrmA输出蛋白发生的。我们得出结论,传感机制区分饥饿和可以向AreA转录因子发出信号的潜在营养物质的存在。氮源的可用性而非质量会通过调节AreA的核出口而影响核积累,从而对养分供应的变化提供快速响应。

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