细胞质膜区域极性化对调控细胞的极性生长和功能分化具有重要作用。花粉管高度依赖顶端膜ROP1和侧面膜REN4相互抑制维持其快速顶端生长，但花粉管如何调节REN4-ROP1作用途径的信号通路至今尚不清楚。通过IP-MS分析，本课题组在花粉管中检测到胞内蛋白激酶RIK1能与REN4互作。RIK1与REN4呈共表达/共定位的线性关系，突变体rik1的花粉管萌发和极性生长缺陷与ren4高度一致，均表现为花粉管过早萌发、低浓度LatB诱导后的去极性化生长缺陷；进一步研究发现RIK1突变导致花粉管ROP1活性的增加及REN4功能下调。由此推测RIK1与REN4-ROP1处于同一信号通路，共同调控花粉管的顶端极性生长。本项目拟通过分子遗传学、细胞生物学、生物化学等方面的研究，以阐明RIK1介导REN4-ROP1信号通路的分子作用机制，为细胞侧面膜与顶端膜极性分布的动态维持机制提供新的理论依据。

The establishment and maintenance of polar domain is critical for cell polarity growth and functional differentiation. Pollen tube tip growing is relied on the dynamic and tight coordination between the apical ROP1 and lateral REN4. However, it is unclear how pollen tubes modulate REN4-ROP1 signaling for its self-sustained growth. Here, we identified cytoplasmic protein kinase RIK1 as REN4 interactor by IP-MS analysis. RIK1 shows coexpression and colocalizion with REN4 in mature pollen and pollen tube. rik1 mimics ren4 in pollen tube premature germination and low dosage LatB-induced depolarized growth. The mutation of RIK1 caused the compromise of REN4 function and further depolarized growth of ROP1 overexpressed pollen tube. Hence, we hypothesized that RIK1 is involved in the REN4-ROP1 pathway for pollen tube tip and polar growth. Our study will uncover a novel RIK1 protein kinase mediated REN4-ROP1 signaling pathway for the dynamic polar maintenance of apical and lateral plasma membrane in tip growth pollen tube.