FLS2 Is a CDK-like Kinase That Directly Binds IFT70 and Is Required for Proper Ciliary Disassembly in Chlamydomonas

PLoS Genet. 2020 Mar 5;16(3):e1008561. doi: 10.1371/journal.pgen.1008561. eCollection 2020 Mar.


Intraflagellar transport (IFT) is required for ciliary assembly and maintenance. While disruption of IFT may trigger ciliary disassembly, we show here that IFT mediated transport of a CDK-like kinase ensures proper ciliary disassembly. Mutations in flagellar shortening 2 (FLS2), encoding a CDK-like kinase, lead to retardation of cilia resorption and delay of cell cycle progression. Stimulation for ciliary disassembly induces gradual dephosphorylation of FLS2 accompanied with gradual inactivation. Loss of FLS2 or its kinase activity induces early onset of kinesin13 phosphorylation in cilia. FLS2 is predominantly localized in the cell body, however, it is transported to cilia upon induction of ciliary disassembly. FLS2 directly interacts with IFT70 and loss of this interaction inhibits its ciliary transport, leading to dysregulation of kinesin13 phosphorylation and retardation of ciliary disassembly. Thus, this work demonstrates that IFT plays active roles in controlling proper ciliary disassembly by transporting a protein kinase to cilia to regulate a microtubule depolymerizer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arabidopsis Proteins / metabolism*
  • Biological Transport / physiology
  • CDC2 Protein Kinase / metabolism*
  • Cell Cycle / physiology
  • Chlamydomonas / metabolism*
  • Cilia / metabolism*
  • Flagella / metabolism
  • Phosphorylation / physiology
  • Plant Proteins / metabolism*
  • Plants, Genetically Modified / metabolism
  • Protein Kinases / metabolism*
  • Signal Transduction / physiology


  • Arabidopsis Proteins
  • Plant Proteins
  • Protein Kinases
  • FLS2 protein, Arabidopsis
  • CDC2 Protein Kinase

Grant support

This work was supported by the National Key R&D Program of China (2017YFA0503500, 2018YFA0902500) and the National Natural Science Foundation of China (31671387 and 31972888) to JP. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.