纤毛是细胞微管为主组成的细胞结构，行使运动、信号传导的功能。其缺陷可导致人体疾病或发育异常，通称为纤毛病。纤毛的组装需要多种过程参与包括信号分子的调控等。MAPK家族的RCK激酶包括ICK，MAK和MOK。在动物细胞中，它们的缺陷导致纤毛长度增加，但是作用机制不详。在衣藻中，RCK激酶含有两个成员MAPK7和LF4。 LF4的缺陷导致纤毛变长，但是MAPK7的功能和作用机理不详。我们在前期工作中获得了MAPK7的突变体，有趣的是它形成极短的纤毛，说明它具有独特的调控纤毛组装的机制。本工作计划研究MAPK7的分子功能和作用机理。我们计划研究MAPK7突变体纤毛的显微结构，MAPK7在细胞和纤毛中的分布和精细定位，在纤毛组装过程中表达以及激酶活性的变化，激酶活性和重要结构域对纤毛组装的影响，上游激酶的鉴定，作用底物的鉴定以及MAPK7和LF4的双突变对纤毛组装的影响，揭示纤毛组装新的分子机制。

Cilia are microtubule-based cellular structures that play essential roles in cell motility and signaling. Ciliary defects are associated with various human diseases and/or developmental defects, termed ciliopathies. Multiple cellular processes are coordinated to participate in ciliary assembly including signaling regulation. RCK is a subfamily of the MAPK family which includes ICK, MAK and MOK, defects of which induce abnormal long cilia in mammals. But the molecular mechanisms are not well understood. In Chlamydomonas, RCKs have only two members including MAPK7 and LF4. Though LF4 is known to inhibit ciliary growth, the function and mechanism of MAPK7 is elusive. We have identified a mapk7 mutant. Of particular interest, this mutant forms extreme short cilia, indicating that MAPK7 promotes ciliary assembly in a novel manner. We propose to study the EM structure of mapk7 cilia, the distribution and precise cellular localization of MAPK7, dynamic changes of its activity and expression during ciliary assembly, the function of the kinase activity and import domains, identification of the upstream kinase and downstream substrates, and characterize the ciliary phenotype of lf4/mapk7 double mutant. We aim to reveal novel mechanisms of ciliary assembly.