Regulation of ROP signaling in cell division and cell expansion by a small ROPGAP family

细胞极性的建立是细胞形态发生的先决条件，细胞内容物的不均匀分布是细胞形态发生的先决条件。细胞的极性受遗传控制，并在细胞、组织和器官水平上进行协调，以确保功能植物器官的刻板复制。植物Rho(ROP)小胞质GTP酶是进化保守的家族，在细胞极性信号传递中起着分子开关的作用，并协调细胞内容物的时空分布。调节蛋白使小的Rho-GTP酶在活性和非活性之间进行切换。鸟苷核苷酸交换因子(Ropgef)，取代鸟苷二磷酸(GDP)为鸟苷三磷酸(GTP)，以促进ROP的激活。相反，GTP酶激活蛋白(RopGAP)加速了GTP固有的缓慢水解，使各自的靶标Rop失活。对ROP失活的调控知之甚少。我们之前对PHGAP亚家族RopGAP的ROP失活的研究表明，它们与细胞分裂有关。它们定位于质膜和分裂部位，需要运动蛋白Kinesin-12 POK才能在该部位保留。我们假设PHGAP在特定的Rop失活过程中起作用，以建立分裂位点/肌动蛋白耗尽区，以确保正常的细胞分裂。我们将进一步深入了解PHGAP在细胞分裂过程中的调控和细胞动力学。我们将阐明哪些ROP被PHGAP失活，我们将寻找新的相互作用伙伴来研究PHGAP蛋白的功能是如何调节的。此外，我们将建立瞬时重建分析来重建ROP信号模块，并研究它们的时空调节。

The establishment of cell polarity, an unequal distribution of cellular content, is a prerequisite of cellular morphogenesis. Cell polarity is under genetic control and coordinated at the cell-, tissue- and organ- level, to ensure the stereotypic reproduction of functional plant organs. The evolutionary conserved family of Rho of plant (ROP) small cytosolic GTPases serves as molecular switches in cell polarity signaling and orchestrate the spatio-temporal distribution of cellular content. Regulatory proteins enable the switching between activity and inactivity of the small Rho-GTPases. The Guanine nucleotide exchange factors (RopGEF), replace guanosin diphosphate (GDP) for guanosine triphosphate (GTP) to promote ROP activation. On the contrary, GTPase activating proteins (RopGAP) accelerate the intrinsically slow hydrolysis of GTP and render the respective target ROPs inactive. Little is known about the regulation of ROP-inactivation. Our previous work on ROP inactivation by the PHGAP subfamily of RopGAPs, implicated them in cell division. They localize to the plasma membrane and the division site and require the motor-protein kinesin-12 POK for retention at that site. We hypothesis that PHGAPs act in the inactivation of specific ROPs to set up the division site/actin depleted zone to ensure normal cell division. We will gain further insights into the regulation and cellular dynamic of PHGAPs during cell division. We will clarify which ROPs are inactivated by PHGAPs and we will identify novel interaction partners to investigate how PHGAP protein function is regulated. In addition we will establish transient reconstitution assays to recreate ROP-signaling modules and investigate their spatio-temporal regulation.