Molecular and functional analysis of the mechanism driving cytoplasmic streaming in Arabidopsis thaliana

胞质流动对于细胞内化合物的分布或它们在细胞中的战略定位是重要的。在植物中，细胞质流动由肌球蛋白控制。讨论了三种类型的原理：通过与肌球蛋白的特定相互作用来动员每种细胞化合物，少数细胞器/RNPs的动员，以及通过某些细胞器/RNPs的缔合和搅拌使其他细胞器/RNPs的共凝性。为了解决这个问题，我们在一个几乎没有细胞质流动的拟南芥突变体(mya1 mya2 xi-k)中表达了融合到特定锚定的肌球蛋白。表达肌球蛋白锚定蛋白但不表达阴性对照的突变肌球蛋白系携带YFP-YFP而不是锚定蛋白，显示出生长挽救。我们建议利用这些品系来研究不同细胞器/RNPs拯救细胞质流动的能力。此外，我们还将通过研究细胞形态发生表型的挽救、肌动蛋白细胞骨架的组织挽救和根毛中的ROP2信号转导来评估不同细胞器/RNPs的运动的生物学意义。

Cytoplasmic streaming is important to distribute intracellular compounds or for their strategic positioning in the cell. In plants, cytoplasmic streaming is governed by myosins. Three types of principles have been discussed: the mobilization of each cellular compound through specific interactions with myosins, the mobilization of few organelles/RNPs and comobilization of others by association and stirring of the liquid phase by some organelles/RNPs. To address this, we have expressed myosins fused to specific anchors in an Arabidopsis mutant (mya1 mya2 xi-k) that exhibits virtually no cytoplasmic streaming. Mutant myosin lines expressing myosin-anchor proteins but not lines expressing the negative control carrying an YFP-YFP instead of an anchor show growth rescue. We propose to use these lines to study the ability of different organelles/RNPs to rescue cytoplasmic streaming. In addition we will assess the biological significance of the movement of different organelles/RNPs by studying the rescue of the cell morphogenesis phenotypes, the rescue of the organization of the actin cytoskeleton and ROP2 signaling in root hairs in mutant and rescued lines.