Persistent activation by constitutive Ste7 promotes Kss1-mediated invasive growth but fails to support Fus3-dependent mating in yeast
Persistent activation by constitutive Ste7 promotes Kss1-mediated invasive growth but fails to support Fus3-dependent mating in yeast
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DOI：
10.1128/mcb.24.20.9221-9238.2004
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发表时间：
2004-10-01
影响因子：
5.3
通讯作者：
Errede, B
中科院分区：
文献类型：
--
作者：
Maleri, S;Ge, QY;Errede, B
丝裂原活化蛋白激酶激酶激酶- ste11 （MAPKKK-Ste11）、MAPKK-Ste7和MAPK-Kss1介导信息素诱导的交配分化和营养响应性侵入性生长。交配途径也需要支架- ste5和额外的MAPK-Fus3。该系统特异性的一个贡献被认为来自于刺激依赖性的MAPK级联募集到上游激活因子，这些激活因子在一个或另一个途径中是独一无二的。为了验证这一前提，我们提出了一个问题，即组成型Ste7的非刺激信号传导是否会导致生物特异性的丧失。相反，我们发现构成型Ste7在不支持交配反应的情况下促进入侵。这种特异性的发生是因为组成型Ste7在体内激活Kss1，而不是Fus3，并促进丝化基因的表达而抑制交配基因的表达。组成型Ste7变异结合mapk和Ste5的能力差异解释了Kss1的选择性激活。这些发现支持了Fus3在体内激活需要结合Ste7和支架-Ste5，但Kss1激活独立于Ste5的模型。这种不依赖于支架的Kss1由组成型Ste7激活，以及通路特异性启动子歧视机制的存在，决定了其独特的发育命运，不受任何显著的外部刺激的影响。
Mitogen-activated protein kinase kinase kinase-Ste11 (MAPKKK-Ste11), MAPKK-Ste7, and MAPK-Kss1 mediate pheromone-induced mating differentiation and nutrient-responsive invasive growth in Saccharomyces cerevisiae. The mating pathway also requires the scaffold-Ste5 and the additional MAPK-Fus3. One contribution to specificity in this system is thought to come from stimulus-dependent recruitment of the MAPK cascade to upstream activators that are unique to one or the other pathway. To test this premise, we asked if stimulus-independent signaling by constitutive Ste7 would lead to a loss of biological specificity. Instead, we found that constitutive Ste7 promotes invasion without supporting mating responses. This specificity occurs because constitutive Ste7 activates Kss1, but not Fus3, in vivo and promotes filamentation gene expression while suppressing mating gene expression. Differences in the ability of constitutive Ste7 variants to bind the MAPKs and Ste5 account for the selective activation of Kss1. These findings support the model that Fus3 activation in vivo requires binding to both Ste7 and the scaffold-Ste5 but that Kss1 activation is independent of Ste5. This scaffold-independent activation of Kss1 by constitutive Ste7 and the existence of mechanisms for pathway-specific promoter discrimination impose a unique developmental fate independently of any distinguishing external stimuli.