Evidence that the Dictyostelium Dd-STATa protein is a repressor that regulates commitment to stalk cell differentiation and is also required for efficient chemotaxis.
Evidence that the Dictyostelium Dd-STATa protein is a repressor that regulates commitment to stalk cell differentiation and is also required for efficient chemotaxis.
复制标题
有证据表明盘基网柄菌 Dd-STATa 蛋白是一种阻遏蛋白，可调节茎细胞分化，也是有效趋化性所必需的。
作者：
Sudhasri Mohanty;K. Jermyn;A. Early;T. Kawata;Laurence Aubry;A. Ceccarelli;Pauline Schaap;Jeffrey G. Williams;R. Firtel
Dd-STATa是后生动物STAT（信号转导和转录激活因子）蛋白的结构和功能同源物。我们发现，Dd-STATa空细胞表现出几种不同的发育表型。Dd-STATa空细胞的聚集被延迟，并且它们缓慢地向环AMP源化学转运，这表明Dd-STATa在这些早期过程中的作用。在Dd-STATa缺失菌株中，形成了蛞蝓样结构，但它们具有异常的基因表达模式。在这种蛞蝓中，ecmB/lacZ，一种通常对茎细胞分化途径上的细胞具有特异性的标记物，在整个前茎区域表达。网柄藻的茎细胞分化被认为是负调控的，由茎细胞特异性基因启动子中的阻遏元件介导。Dd-STATa在体外结合这些阻遏物元件，并且在无效菌株中ecmB/lacZ的异位表达提供了体内证据，即Dd-STATa是调节柄细胞分化定型的阻遏物蛋白。Dd-STATa缺失细胞在单层测定中显示异常行为，其中使用柄细胞形态原DIF诱导柄细胞分化。在Dd-STATa缺失细胞中，DIF极大地过度诱导了作为茎细胞分化的一般标记的ecmB基因。此外，Dd-STATa无效细胞对DIF表达ST/lacZ（一种茎细胞亚型之一分化的最早阶段的标志物）超敏感。我们认为，这两种表现DIF超敏反应的无效菌株的结果之间的平衡激活和抑制的启动子元件被倾斜，有利于激活时，阻遏物是缺席。有趣的是，虽然Dd-STATa null细胞对DIF的诱导作用非常敏感，并且在单层测定中容易形成柄细胞，但Dd-STATa null细胞在蛞蝓中显示很少或没有终末柄细胞分化。Dd-STATa无效蛞蝓在形成由一列明显未分化的细胞支持的非常小的孢子团之前保持发育停滞数天。因此，完整的茎细胞分化似乎需要至少两个事件：定型步骤，其中Dd-STATa施加的抑制被解除，以及在Dd-STATa无效生物体中被阻断的第二步骤。这后一步可能涉及细胞外cAMP，一种已知的柄细胞分化的阻遏物，因为Dd-STATa无效细胞对细胞外环AMP的抑制作用异常敏感。
Dd-STATa is a structural and functional homologue of the metazoan STAT (Signal Transducer and Activator of Transcription) proteins. We show that Dd-STATa null cells exhibit several distinct developmental phenotypes. The aggregation of Dd-STATa null cells is delayed and they chemotax slowly to a cyclic AMP source, suggesting a role for Dd-STATa in these early processes. In Dd-STATa null strains, slug-like structures are formed but they have an aberrant pattern of gene expression. In such slugs, ecmB/lacZ, a marker that is normally specific for cells on the stalk cell differentiation pathway, is expressed throughout the prestalk region. Stalk cell differentiation in Dictyostelium has been proposed to be under negative control, mediated by repressor elements present in the promoters of stalk cell-specific genes. Dd-STATa binds these repressor elements in vitro and the ectopic expression of ecmB/lacZ in the null strain provides in vivo evidence that Dd-STATa is the repressor protein that regulates commitment to stalk cell differentiation. Dd-STATa null cells display aberrant behavior in a monolayer assay wherein stalk cell differentiation is induced using the stalk cell morphogen DIF. The ecmB gene, a general marker for stalk cell differentiation, is greatly overinduced by DIF in Dd-STATa null cells. Also, Dd-STATa null cells are hypersensitive to DIF for expression of ST/lacZ, a marker for the earliest stages in the differentiation of one of the stalk cell sub-types. We suggest that both these manifestations of DIF hypersensitivity in the null strain result from the balance between activation and repression of the promoter elements being tipped in favor of activation when the repressor is absent. Paradoxically, although Dd-STATa null cells are hypersensitive to the inducing effects of DIF and readily form stalk cells in monolayer assay, the Dd-STATa null cells show little or no terminal stalk cell differentiation within the slug. Dd-STATa null slugs remain developmentally arrested for several days before forming very small spore masses supported by a column of apparently undifferentiated cells. Thus, complete stalk cell differentiation appears to require at least two events: a commitment step, whereby the repression exerted by Dd-STATa is lifted, and a second step that is blocked in a Dd-STATa null organism. This latter step may involve extracellular cAMP, a known repressor of stalk cell differentiation, because Dd-STATa null cells are abnormally sensitive to the inhibitory effects of extracellular cyclic AMP.
盘基网柄菌中三种 cAMP 受体的环核苷酸特异性。
DOI：
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发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
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作者：
Johnson,RL;VanHaastert,PJ;Kimmel,AR;Saxe3rd,CL;Jastorff,B;Devreotes,PN
通讯作者：
Devreotes,PN
盘基网柄菌中的跨膜信号传导。
影响因子：
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作者：
Devreotes,P;Fontana,D;Klein,P;Sherring,J;Theibert,A
通讯作者：
Theibert,A