The role of Actin dynamics in auxin-dependent oriented cell division

植物细胞被限制其运动的刚性壁包围，因此定向细胞分裂是在生长和发育期间定义形状的中心机制。定向分裂是胚胎和胚后发育过程中形成细胞多样性的基础。尽管对内在细胞分裂机制有详细的了解，但细胞分裂的方向是如何由发育调节因子控制的还完全不清楚。世纪的经典模型预测细胞的几何形状通过一个简单的物理规则来限制分裂平面。最近的研究表明，这种几何默认规则确实可以解释早期拟南芥胚胎在3D中的许多分裂。然而，所有不对称的划分都违反了这一规则。研究表明，抑制默认分裂需要对生长素激素的转录应答。对这种抑制的分子调节的进一步分析揭示了多种肌动蛋白调节剂。在这个项目中，我将使用遗传学，细胞生物学，分子和计算相结合的方法来解决1）肌动蛋白模式在胚胎发育过程中如何变化，以及它们与定向细胞分裂相关，以及2）哪些蛋白质调节早期胚胎中的肌动蛋白动力学。此外，我将探讨在控制定向细胞分裂中，肌动蛋白调节是否介导生长素的作用。我希望这个项目的成果将发育调节因子与细胞分裂机制联系起来，从而填补我们关于超细胞发育如何实施到单个细胞行为的知识中的一个主要空白。

Plant cells are surrounded by rigid walls restricting their movement, and therefore oriented cell division is a central mechanism in defining shape during growth and development. Oriented divisions underlie formative events during embryonic and post-embryonic development to generate cell diversity. Despite detailed knowledge of the intrinsic cell division machinery, it is entirely unclear how orientation of cell divisions is controlled by developmental regulators. Classical models in the 19th century predicted that cell geometry constrains division plane through a simple physical rule. It was recently demonstrated that this geometric default rule can indeed explain many divisions in the early Arabidopsis embryo in 3D. However, all asymmetric divisions disobeyed this rule. It was shown that transcriptional response to the auxin hormone is required to suppress default division. Further analysis on the molecular regulation for this suppression revealed multiple Actin regulators. In this project, I will use a combined genetic, cell biological, molecular and computational approach to address 1) how Actin patterns change during embryo development, and do they correlate with oriented cell division, and 2) which proteins regulate Actin dynamics in the early embryo. Furthermore, I will 3) explore whether Actin regulation mediates auxin action in controlling oriented cell division. I expect the outcomes of this project to connect developmental regulators to the cell division machinery and thus to fill a major gap in our knowledge on how supracellular development is implemented into individual cell behaviour.