Yeh Brian J, Rutigliano Robert J, Deb Anrica, Bar-Sagi Dafna, Lim Wendell A
Chemistry and Chemical Biology Graduate Program, University of California, San Francisco, San Francisco, California 94158-2517, USA.
Nature. 2007 May 31;447(7144):596-600. doi: 10.1038/nature05851. Epub 2007 May 21.
Eukaryotic cells mobilize the actin cytoskeleton to generate a remarkable diversity of morphological behaviours, including motility, phagocytosis and cytokinesis. Much of this diversity is mediated by guanine nucleotide exchange factors (GEFs) that activate Rho family GTPases-the master regulators of the actin cytoskeleton. There are over 80 Rho GEFs in the human genome (compared to only 22 genes for the Rho GTPases themselves), and the evolution of new and diverse GEFs is thought to provide a mechanism for linking the core cytoskeletal machinery to a wide range of new control inputs. Here we test this hypothesis and ask if we can systematically reprogramme cellular morphology by engineering synthetic GEF proteins. We focused on Dbl family Rho GEFs, which have a highly modular structure common to many signalling proteins: they contain a catalytic Dbl homology (DH) domain linked to diverse regulatory domains, many of which autoinhibit GEF activity. Here we show that by recombining catalytic GEF domains with new regulatory modules, we can generate synthetic GEFs that are activated by non-native inputs. We have used these synthetic GEFs to reprogramme cellular behaviour in diverse ways. The GEFs can be used to link specific cytoskeletal responses to normally unrelated upstream signalling pathways. In addition, multiple synthetic GEFs can be linked as components in series to form an artificial cascade with improved signal processing behaviour. These results show the high degree of evolutionary plasticity of this important family of modular signalling proteins, and indicate that it may be possible to use synthetic biology approaches to manipulate the complex spatio-temporal control of cell morphology.
真核细胞通过肌动蛋白细胞骨架产生多种显著不同的形态学行为,包括运动性、吞噬作用和胞质分裂。这种多样性很大程度上是由鸟嘌呤核苷酸交换因子(GEFs)介导的,这些因子激活Rho家族GTP酶——肌动蛋白细胞骨架的主要调节因子。人类基因组中有80多种Rho GEF(相比之下,Rho GTP酶本身只有22个基因),新的和多样化的GEF的进化被认为提供了一种机制,将核心细胞骨架机制与广泛的新控制输入联系起来。在这里,我们检验这一假设,并询问是否可以通过设计合成GEF蛋白来系统地重新编程细胞形态。我们聚焦于Dbl家族Rho GEF,它们具有许多信号蛋白共有的高度模块化结构:它们包含一个与多种调节结构域相连的催化性Dbl同源(DH)结构域,其中许多调节结构域会自动抑制GEF活性。在这里我们表明,通过将催化性GEF结构域与新的调节模块重组,我们可以生成由非天然输入激活的合成GEF。我们已经使用这些合成GEF以多种方式重新编程细胞行为。这些GEF可用于将特定的细胞骨架反应与通常不相关的上游信号通路联系起来。此外,多个合成GEF可以串联作为组件连接起来,形成一个具有改进信号处理行为的人工级联。这些结果显示了这个重要的模块化信号蛋白家族的高度进化可塑性,并表明有可能使用合成生物学方法来操纵细胞形态的复杂时空控制。