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Specificity of MAPK signaling towards FLO11 expression is established by crosstalk from cAMP pathway

机译:通过cAMP通路的串扰确定MAPK信号对FLO11表达的特异性

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摘要

In budding yeast, elements of a single MAP Kinase cascade are shared to regulate a wide range of functions such as mating, differentiation and osmotic stress. However, cells have programmed to execute correct event in response to a given input signal without cross activating other responses. Studies have observed that magnitude and duration of MAPK activation encodes specificity. Similarly, the differential regulation of Tec1p, a transcriptional activator of invasive growth gene, FLO11 by MAP kinases has been observed to bring specificity in mating and invasive growth signaling. However, the understanding of interactions between the shared components and other signaling pathways related to the phenotypic response in contributing towards specificity remains unclear. We specifically address the crosstalk of cAMP pathway with MAPK pathway in haploid invasive growth and show the contribution and importance of cAMP pathway towards invasive growth irrespective of the activation status of MAPK pathway. Our analysis shows that crosstalk from cAMP pathway in haploids might offer an advantage in terms of amplifying the observed weak signaling through MAPK pathway. Further, we show that such a crosstalk in haploids leads to higher FLO11 expression than diploids. We also demonstrate the positive and negative role of Tpk1 and Tpk3 in haploid invasive growth. Finally, we observe that a cross-inhibition at gene level brought about by cAMP pathway controlled inhibitor, Sfl1, perhaps help in deamplifying the MAPK signal and also in preventing FLO11 expression in the absence of cAMP pathway activation.Electronic supplementary materialThe online version of this article (doi:10.1007/s11693-007-9007-7) contains supplementary material, which is available to authorized users.
机译:在发芽酵母中,单个MAP激酶级联的元件被共享以调节广泛的功能,例如交配,分化和渗透胁迫。但是,单元已编程为响应给定的输入信号执行正确的事件,而不会交叉激活其他响应。研究已经观察到MAPK激活的幅度和持续时间编码特异性。同样,已观察到通过MAP激酶对Tec1p(侵袭性生长基因的转录激活因子FLO11)的差异调节,可以在交配和侵袭性生长信号传导中带来特异性。然而,对共享成分与其他与表型反应有关的信号传导途径之间的相互作用的理解尚不清楚。我们专门解决了单倍体侵袭性生长中cAMP途径与MAPK途径的串扰,并显示了cAMP途径对侵袭性生长的贡献和重要性,而与MAPK途径的激活状态无关。我们的分析表明,单倍体中来自cAMP途径的串扰可能在放大通过MAPK途径观察到的微弱信号方面提供优势。此外,我们表明单倍体中的这种串扰比二倍体导致更高的FLO11表达。我们还证明了Tpk1和Tpk3在单倍体侵袭性生长中的正负作用。最后,我们观察到由cAMP途径控制的抑制剂Sfl1在基因水平上产生的交叉抑制作用可能有助于在没有cAMP途径活化的情况下使MAPK信号去扩增并阻止FLO11的表达。文章(doi:10.1007 / s11693-007-9007-7)包含补充材料,授权用户可以使用。

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