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A NIMA-Related Kinase Suppresses the Flagellar Instability Associated with the Loss of Multiple Axonemal Structures
Cilia are specialized projections found on the surface of eukaryotic cells. They play crucial sensory functions, as well as motile functions needed for clearing airways or propelling cells. Ciliary motility is perturbed in the inherited disease, Primary Ciliary Dyskinesia (PCD). Two coiled coil domain-containing (CCDC39 and CCDC40) proteins are needed for the assembly of multiple key structures/complexes that are required for generating ciliary motility. Using the unicellular green alga, Chlamydomonas, we have identified a kinase (CNK11) that when mutated is able to partially rescue the short flagella phenotype of the ccdc39 and ccdc40 mutants as well as mutants lacking axonemal dyneins or the N-DRC complex. In addition, CCDC40 is required for tubulin polyglutamylation at the proximal end of flagella. We suggest that substructures like dynein arms and the N-DRC, which are needed for motility, play a second role in stabilizing the axonemal microtubules and are needed for proper length control. The polyglutamylase, TTLL9, and the kinase, CNK11, play roles in stabilizing the axonemal microtubules based on their ability to partially rescue the short flagella phenotypes of multiple mutants.
Vyšlo v časopise: A NIMA-Related Kinase Suppresses the Flagellar Instability Associated with the Loss of Multiple Axonemal Structures. PLoS Genet 11(9): e32767. doi:10.1371/journal.pgen.1005508
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1005508Souhrn
Cilia are specialized projections found on the surface of eukaryotic cells. They play crucial sensory functions, as well as motile functions needed for clearing airways or propelling cells. Ciliary motility is perturbed in the inherited disease, Primary Ciliary Dyskinesia (PCD). Two coiled coil domain-containing (CCDC39 and CCDC40) proteins are needed for the assembly of multiple key structures/complexes that are required for generating ciliary motility. Using the unicellular green alga, Chlamydomonas, we have identified a kinase (CNK11) that when mutated is able to partially rescue the short flagella phenotype of the ccdc39 and ccdc40 mutants as well as mutants lacking axonemal dyneins or the N-DRC complex. In addition, CCDC40 is required for tubulin polyglutamylation at the proximal end of flagella. We suggest that substructures like dynein arms and the N-DRC, which are needed for motility, play a second role in stabilizing the axonemal microtubules and are needed for proper length control. The polyglutamylase, TTLL9, and the kinase, CNK11, play roles in stabilizing the axonemal microtubules based on their ability to partially rescue the short flagella phenotypes of multiple mutants.
Zdroje
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