Department of Cell and Developmental Biology; Department of Radiology; Witman Lab
Cell Biology | Cellular and Molecular Physiology | Developmental Biology
We have used an insertional mutagenesis approach to generate new C. reinhardtii motility mutants. Of 56 mutants isolated, one is a new allele at the ODA3 locus, called oda3-6. Similar to the previously characterized oda3 alleles, oda3-6 has a slow-jerky swimming phenotype and reduced swimming speed. The oda3-6 mutant fails to assemble the outer dynein arm motor and outer dynein arm-docking complex (ODA-DC) in the ciliary axoneme due to an insertion in the 5' end of the DCC1 gene, which encodes the DC1 subunit of the ODA-DC. Transformation of oda3-6 with the wild-type DCC1 gene rescues the mutant swimming phenotype and restores assembly of the ODA-DC and the outer dynein arm in the cilium. This is the first oda3 mutant to be characterized at the molecular level and is likely to be very useful for further analysis of DC1 function.
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Copyright: © 2017 Brown et al.
DOI of Published Version
PLoS One. 2017 Mar 14;12(3):e0173842. eCollection 2017. Link to article on publisher's site
Brown JM, Mosley M, Montes-Berrueta D, Hou Y, Yang F, Scarbrough C, Witman GB, Wirschell M. (2017). Characterization of a new oda3 allele, oda3-6, defective in assembly of the outer dynein arm-docking complex in Chlamydomonas reinhardtii. Open Access Articles. https://doi.org/10.1371/journal.pone.0173842. Retrieved from https://escholarship.umassmed.edu/oapubs/3050
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