Department of Chemistry, Technische Universität München, Lichtenbergstrasse 4, 85747 Garching, Germany.
J Biol Chem. 2011 Oct 21;286(42):36907-20. doi: 10.1074/jbc.M111.225052. Epub 2011 Aug 16.
Dictyostelium Formin C (ForC) is involved in the regulation of local actin cytoskeleton reorganization (e.g. during cellular adhesion or migration). ForC contains formin homology 2 and 3 (FH2 and -3) domains and an N-terminal putative GTPase-binding domain (GBD) but lacks a canonical FH1 region. To better understand the role of the GBD, its structure, dynamics, lipid-binding properties, and cellular functions were analyzed by NMR and CD spectroscopy and by in vivo fluorescence microscopy. Moreover, the program CS-Rosetta was tested for the structure prediction based on chemical shift data only. The ForC GBD adopts an ubiquitin-like α/β-roll fold with an unusually long loop between β-strands 1 and 2. Based on the lipid-binding data, the presence of DPC micelles induces the formation of α-helical secondary structure and a rearrangement of the tertiary structure. Lipid-binding studies with a mutant protein and a peptide suggest that the β1-β2 loop is not relevant for these conformational changes. Whereas small amounts of negatively charged phosphoinositides (1,2-dioctanoyl-sn-glycero-3-(phosphoinositol 4,5-bisphosphate) and 1,2-dihexanoyl-sn-glycero-3-(phosphoinositol 3,4,5-trisphosphate)) lower the micelle concentration necessary to induce the observed spectral changes, other negatively charged phospholipids (1,2-dihexanoyl-sn-glycero-3-(phospho-L-serine) and 1,2-dihexanoyl-sn-glycero-3-phospho-(1'-rac-glycerol)) had no such effect. Interestingly, bicelles and micelles composed of diacylphosphocholines had no effect on the GBD structure. Our data suggest a model in which part of the large positively charged surface area of the GBD mediates localization to specific membrane patches, thereby regulating interactions with signaling proteins. Our cellular localization studies show that both the GBD and the FH3 domain are required for ForC targeting to cell-cell contacts and early phagocytic cups and macropinosomes.
Dictyostelium 形态发生蛋白 C(ForC)参与调节局部肌动蛋白细胞骨架的重组(例如,在细胞黏附或迁移过程中)。ForC 包含形态发生蛋白同源结构域 2 和 3(FH2 和 -3)以及 N 端假定的 GTP 酶结合结构域(GBD),但缺乏典型的 FH1 区域。为了更好地理解 GBD 的作用,通过 NMR 和 CD 光谱学以及体内荧光显微镜分析了其结构、动力学、脂质结合特性和细胞功能。此外,还使用 CS-Rosetta 程序仅基于化学位移数据进行结构预测。ForC GBD 采用了一种不寻常的长环连接β-链 1 和 2 的泛素样α/β-滚折叠结构。基于脂质结合数据,DPC 胶束的存在诱导形成α-螺旋二级结构和三级结构的重排。用突变蛋白和肽进行的脂质结合研究表明,β1-β2 环与这些构象变化无关。虽然少量带负电荷的磷酸肌醇(1,2-二辛酰基-sn-甘油-3-(磷酸肌醇 4,5-二磷酸)和 1,2-二己酰基-sn-甘油-3-(磷酸肌醇 3,4,5-三磷酸))降低了诱导观察到的光谱变化所需的胶束浓度,但其他带负电荷的磷脂(1,2-二己酰基-sn-甘油-3-(磷酸-L-丝氨酸)和 1,2-二己酰基-sn-甘油-3-磷酸-(1'-rac-甘油))则没有这种作用。有趣的是,双脂胶束和由二酰基磷酸胆碱组成的胶束对 GBD 结构没有影响。我们的数据提出了一个模型,其中 GBD 的部分大的带正电荷表面区域介导定位到特定的膜斑,从而调节与信号蛋白的相互作用。我们的细胞定位研究表明,GBD 和 FH3 结构域对于 ForC 靶向细胞-细胞接触以及早期吞噬小泡和巨胞饮泡都是必需的。