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CCDC39 and CCDC40 were first identified as causative mutations in primary ciliary dyskinesia patients; cilia from patients show disorganized microtubules, and they are missing both N-DRC and inner dynein arms proteins. In  Chlamydomonas , we used immunoblots and microtubule sliding assays to show that mutants in  CCDC40  ( PF7 ) and  CCDC39  ( PF8 ) fail to assemble N-DRC, several inner dynein arms, tektin, and CCDC39. Enrichment screens for suppression of  pf7 ;  pf8  cells led to the isolation of five independent extragenic suppressors defined by four different mutations in a NIMA-related kinase,  CNK11 . These alleles partially rescue the flagellar length defect, but not the motility defect. The suppressor does not restore the missing N-DRC and inner dynein arm proteins. In addition, the  cnk11  mutations partially suppress the short flagella phenotype of N-DRC and axonemal dynein mutants, but do not suppress the motility defects. The  tpg1  mutation in  TTLL9 , a tubulin polyglutamylase, partially suppresses the length phenotype in the same axonemal dynein mutants. In contrast to  cnk11 ,  tpg1  does not suppress the short flagella phenotype of  pf7 . The polyglutamylated tubulin in the proximal region that remains in the  tpg1  mutant is reduced further in the  pf7; tpg1  double mutant by immunofluorescence. CCDC40, which is needed for docking multiple other axonemal complexes, is needed for tubulin polyglutamylation in the proximal end of the flagella. The CCDC39 and CCDC40 proteins are likely to be involved in recruiting another tubulin glutamylase(s) to the flagella. Another difference between  cnk11-1  and  tpg1  mutants is that  cnk11-1  cells show a faster turnover rate of tubulin at the flagellar tip than in wild-type flagella and  tpg1  flagella show a slower rate. The double mutant shows a turnover rate similar to  tpg1 , which suggests the faster turnover rate in  cnk11-1  flagella requires polyglutamylation. Thus, we hypothesize that many short flagella mutants in  Chlamydomonas  have increased instability of axonemal microtubules. Both CNK11 and tubulin polyglutamylation play roles in regulating the stability of axonemal microtubules.

A NIMA-Related Kinase Suppresses the Flagellar Instability Associated with the Loss of Multiple Axonemal Structures