Cilia and flagella are evolutionarily conserved,microtubule-based organelles on the surface of most eukaryotic cells.They play important roles in coordinating a variety of signaling pathways during growth,development,cell mobility,and tissue homeostasis.Defects in ciliary structure or function are associated with multiple human disorders called ciliopathies.Cilia and flagella are dynamic organelles that undergo assembly and disassembly during cell cycle.The mechanisms by which these organelles are disassembled are incompletely understood.We used insertional mutagenesis to identify genes required for flagella disassembly in Chlamydomonas and obtained a flagellar shortening defect mutant fls2.The mutant cells exhibited long flagella and show shortening defects during flagellar resorption.It also has a delay in cell division of about 1.5h compared to WT control cells.FLS2 is primarily localized to the axoneme and transported into flagella by intraflagellar transport complex.We demonstrated that FLS2 protein interacts with IFT70 by yeast two hybrid.Mechanistically,loss of function of FLS2 has an impact on phosphorylation of CrKinesinl3,a microtubule depolymerase,which is involved in flagellar shortening.Further more,to determine whether the kinase activity of FLS2 was required for flagellar shortening,fls2 was transformed with HA-tagged kinase-dead mutant (K33R) of FLS2.We found that the kinase activity has no impact on the location and transport,but affects the phosphorylation of CrKinesinl3.The results demonstrate that the kinase activity of FLS2 is required.