DRC3 connects the N-DRC to dynein g to regulate flagellar waveform

Junya Awata, Kangkang Song, Jianfeng Lin, Stephen M. King, Michael J. Sanderson, Daniela Nicastro, George B. Witman

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


The nexin-dynein regulatory complex (N-DRC), which is a major hub for the control of flagellar motility, contains at least 11 different subunits. A major challenge is to determine the location and function of each of these subunits within the N-DRC. We characterized a Chlamydomonas mutant defective in the N-DRC subunit DRC3. Of the known N-DRC subunits, the drc3 mutant is missing only DRC3. Like other N-DRC mutants, the drc3 mutant has a defect in flagellar motility. However, in contrast to other mutations affecting the N-DRC, drc3 does not suppress flagellar paralysis caused by loss of radial spokes. Cryo-electron tomography revealed that the drc3 mutant lacks a portion of the N-DRC linker domain, including the L1 protrusion, part of the distal lobe, and the connection between these two structures, thus localizing DRC3 to this part of the N-DRC. This and additional considerations enable us to assign DRC3 to the L1 protrusion. Because the L1 protrusion is the only nondynein structure in contact with the dynein g motor domain in wild-type axonemes and this is the only N-DRC-dynein connection missing in the drc3 mutant, we conclude that DRC3 interacts with dynein g to regulate flagellar waveform.

Original languageEnglish (US)
Pages (from-to)2788-2800
Number of pages13
JournalMolecular biology of the cell
Issue number15
StatePublished - Aug 1 2015

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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