Microarray phenotyping places cyclase associated protein CAP at the crossroad of signaling pathways reorganizing the actin cytoskeleton in Dictyostelium.
Microarray phenotyping places cyclase associated protein CAP at the crossroad of signaling pathways reorganizing the actin cytoskeleton in Dictyostelium.
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微阵列表型分析将环化酶相关蛋白 CAP 置于重组网柄菌肌动蛋白细胞骨架的信号通路的十字路口
DOI：
10.1016/j.yexcr.2008.10.023
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发表时间：
2009
影响因子：
3.7
通讯作者：
Noegel
中科院分区：
文献类型：
--
作者：
Sultana;Neelakanta;Eichinger;Rivero;Noegel
大规模的基因表达分析最近已被应用于发现在特定过程中共调控的基因组。在这里，我们进行这样的分析CAP，蛋白质参与调节的肌动蛋白细胞骨架和cAMP信号在网骨藻。微阵列分析显示CAP的缺失改变了许多细胞骨架成分的表达。进一步分析其中之一，Rho GDP解离抑制剂RhoGDI 1。RhoGDI 1空细胞表达较低量的CAP，其未能主要在细胞皮层积累。为了进一步定位CAP在相应的信号转导途径，我们研究了CAP定位和细胞功能的突变体，有缺陷的几个信号传导组件。CAP在所有分析的菌株中显示出正确的定位和动力学，除了在缺乏cAMP依赖性蛋白激酶A活性的突变体中，CAP优先积累在冠状结构中。CAP的异位表达提高了Gβ缺陷细胞的吞噬效率，并恢复了PI 3激酶双突变体（pi 3 k1/2 null）的胞饮、形态和肌动蛋白分布缺陷。我们的研究结果表明，CAP的行为在多个十字路口，并链接到肌动蛋白细胞骨架的信号通路，无论是通过物理相互作用与细胞骨架成分或通过调节其基因表达。
Large-scale gene expression analysis has been applied recently to uncover groups of genes that are co-regulated in particular processes. Here we undertake such an analysis on CAP, a protein that participates in the regulation of the actin cytoskeleton and in cAMP signaling in Dictyostelium. microarray analysis revealed that loss of CAP altered the expression of many cytoskeletal components. One of these, the Rho GDP-dissociation inhibitor RhoGDI1, was analyzed further. RhoGDI1 null cells expressed lower amounts of CAP, which failed to accumulate predominantly at the cell cortex. To further position CAP in the corresponding signal transduction pathways we studied CAP localization and cellular functioning in mutants that have defects in several signaling components. CAP showed correct localization and dynamics in all analyzed strains except in mutants with deficient cAMP dependent protein kinase A activity, where CAP preferentially accumulated in crown shaped structures. Ectopic expression of CAP improved the efficiency of phagocytosis in Gβ-deficient cells and restored the pinocytosis, morphology and actin distribution defects in a PI3 kinase double mutant (pi3k1/2 null). Our results show that CAP acts at multiple crossroads and links signaling pathways to the actin cytoskeleton either by physical interaction with cytoskeletal components or through regulation of their gene expression.
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