花粉萌发对植物的繁殖至关重要。在萌发过程中，依赖于formin的肌动蛋白聚合在囊泡运输和极性建立中起着重要作用。然而，formin介导的肌动蛋白组装及囊泡运输在体内的调节机制尚不清楚。本课题中，我们探究了生殖型profilins(PRF4和PRF5)在花粉萌发极性建立过程中的作用。发现prf4 prf5-1双突变体花粉粒中微丝含量降低，过表达PRF4和PRF5导致花粉粒中微丝含量显著增加，表明profilin在花粉粒内能够促进微丝聚合。然而，在AtFH5突变体atfh5-3中，profilin促进肌动蛋白聚合的积极作用不复存在，且PRF5与PLP互作的关键位点突变后同样不能促进微丝聚合。进一步的体外生化实验结果表明profilin自身不能促进肌动蛋白组装，而是与AtFH5共同协作加速微丝的成核和延伸。这些结果表明，PRF4、PRF5在花粉粒中促进微丝聚合的能力依赖于与AtFH5的相互作用。此外，prf4 prf5-1花粉粒中AtFH5标记囊泡的运输减慢且出现了断断续续的现象，花粉萌发孔的微丝环状结构也存在缺陷，萌发初期的微丝环状结构无法稳定在花粉管的亚顶端，以上结果均与profilin含量下降后微丝的快速延伸受到了影响、AtFH5与微丝正端的相互作用减弱有关。综上所述，我们的结果表明，PRF4和PRF5通过促进AtFH5介导的肌动蛋白聚合和增强AtFH5与微丝之间的相互作用来调节花粉萌发过程中的囊泡运输和极性建立。

Pollen germination is very important for the reproduction of flowering plants. Formin-dependent actin polymerization plays vital roles in vesicle trafficking and polarity establishment during this process. However, how formin-mediated actin assembly is regulated in vivo remains poorly understood. Here, we investigated the function of reproductive profilins (PRF4 and 5) in the polarity establishment process during pollen germination. Our data showed that the actin filament content decreased in the prf4 prf5 double mutant and increased significantly in both PRF4- and PRF5-overexpressing pollen grains. In contrast, the positive effect of profilin in promoting actin polymerization was abolished in a formin mutant, atfh5-3. In addition, the interaction between AtFH5 and actin filaments was attenuated and the trafficking of AtFH5-labeled vesicles was slowed in prf4 prf5 pollen grains. Formation of the collar-like-structure at the germination pore was also defective in prf4 prf5 pollen grains as the fast assembly of actin filaments was impaired. Together, our results suggest that PRF4 and PRF5 regulate vesicle trafficking and polarity establishment during pollen germination by promoting AtFH5-mediated actin polymerization and enhancing the interaction between AtFH5 and actin filaments.