Little is known about the molecular basis of organelle size control in eukaryotes. Cells of the biflagellate alga Chlamydomonas reinhardtii actively maintain their flagella at a precise length. Chlamydomonas mutants that lose control of flagellar length have been isolated and used to demonstrate that a dynamic process keeps flagella at an appropriate length [1, 2]. To date, none of the proteins required for flagellar length control have been identified in any eukaryotic organism. Here, we show that a novel MAP kinase is crucial to enforcing wild-type flagellar length in C. reinhardtii. Null mutants of LF4 , a gene encoding a protein with extensive amino acid sequence identity to a mammalian MAP kinase of unknown function, MOK , are unable to regulate the length of their flagella. The LF4 protein (LF4p) is localized to the flagella, and in vitro enzyme assays confirm that the protein is a MAP kinase. The long-flagella phenotype of If4 cells is rescued by transformation with the cloned LF4 gene. The demonstration that a novel MAP kinase helps enforce flagellar length control indicates that a previously unidentified signal transduction pathway controls organelle size in C. reinhardtii.
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We thank our collegues in the Chlamydomonas community, including Drs. Gregory Pazour, David Mitchell, Carl Johnson, and Carolyn Silflow, for providing LF4 strains. We thank Drs. Rachel Nguyen, Lai-Wa Tam, and Carolyn Silflow for helpful discussions. This work was supported by National Institute of General Medical Sciences Grant GM34437 to P.A.L., National Institutes of Health Post-Doctoral Fellowship 5F32-GM20149 to N.F.W., and the Plant Molecular Genetics Institute of the University of Minnesota.