PHOSPHOREGULATION OF AN INNER DYNEIN ARM COMPLEX IN CHLAMYDOMONAS-REINHARDTII IS ALTERED IN PHOTOTACTIC MUTANT STRAINS

To gain a further understanding of axonemal dynein regulation, mutant strains of Chlamydomonas reinhardtii that had defects in both phototac tic behavior and flagellar motility were identified and characterized. ptm1, ptm2, and ptm3 mutant strains exhibited motility phenotypes tha t resembled those of known inner dynein arm region mutant strains, but did not have biochemical or genetic phenotypes characteristic of othe r inner dynein arm mutations. Three other mutant strains had defects i n the f class of inner dynein arms. Dynein extracts from the pf9-4 str ain were missing the entire f complex. Strains with mutations in pf9/i da1, ida2, or ida3 failed to assemble the f dynein complex and did not exhibit phototactic behavior. Fractionated dynein from mia1-1 and mia 2-1 axonemes exhibited a novel f class inner dynein arm biochemical ph enotype; the 138-kD f intermediate chain was present in altered phosph orylation forms. In vitro axonemal dynein activity was reduced by the mia1-1 and mia2-1 mutations. The addition of kinase inhibitor restored axonemal dynein activity concomitant with the dephosphorylation of th e 138-kD f intermediate chain. Dynein extracts from uni1-1 axonemes, w hich specifically assemble only one of the two flagella, contained rel atively high levels of the altered phosphorylation forms of the 138-kD intermediate chain. We suggest that the f dynein complex may be phosp horegulated asymmetrically between the two flagella to achieve photota ctic turning.