Higaki Takumi, Kutsuna Natsumaro, Akita Kae, Takigawa-Imamura Hisako, Yoshimura Kenji, Miura Takashi
Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Research and Development Division, LPixel Inc., Tokyo, Japan.
PLoS Comput Biol. 2016 Apr 7;12(4):e1004833. doi: 10.1371/journal.pcbi.1004833. eCollection 2016 Apr.
Plant leaf epidermal cells exhibit a jigsaw puzzle-like pattern that is generated by interdigitation of the cell wall during leaf development. The contribution of two ROP GTPases, ROP2 and ROP6, to the cytoskeletal dynamics that regulate epidermal cell wall interdigitation has already been examined; however, how interactions between these molecules result in pattern formation remains to be elucidated. Here, we propose a simple interface equation model that incorporates both the cell wall remodeling activity of ROP GTPases and the diffusible signaling molecules by which they are regulated. This model successfully reproduces pattern formation observed in vivo, and explains the counterintuitive experimental results of decreased cellulose production and increased thickness. Our model also reproduces the dynamics of three-way cell wall junctions. Therefore, this model provides a possible mechanism for cell wall interdigitation formation in vivo.
植物叶片表皮细胞呈现出一种类似拼图的模式,这种模式是在叶片发育过程中由细胞壁的相互交错形成的。已经研究了两种ROP GTP酶(ROP2和ROP6)对调节表皮细胞壁相互交错的细胞骨架动力学的贡献;然而,这些分子之间的相互作用如何导致模式形成仍有待阐明。在这里,我们提出了一个简单的界面方程模型,该模型既包含了ROP GTP酶的细胞壁重塑活性,也包含了它们所受调控的可扩散信号分子。该模型成功地再现了体内观察到的模式形成,并解释了纤维素产量降低和厚度增加这一违反直觉的实验结果。我们的模型还再现了三向细胞壁连接的动力学。因此,该模型为体内细胞壁相互交错的形成提供了一种可能的机制。