PubMed ID
10512883
UMMS Affiliation
Department of Cell Biology; Program in Molecular Medicine
Date
10-8-1999
Document Type
Article
Subjects
Animals; Cell Movement; Chlamydomonas reinhardtii; Cloning, Molecular; Dynein ATPase; Flagella; *Genes, Protozoan; *Intracellular Signaling Peptides and Proteins; Mice; Microscopy, Electron; *Microtubule-Associated Proteins; Microtubules; Mutation; Nuclear Proteins; Phenotype; Protozoan Proteins; Sequence Homology; Transformation, Genetic
Disciplines
Life Sciences | Medicine and Health Sciences
Abstract
Tctex2 is thought to be one of the distorter genes of the mouse t haplotype. This complex greatly biases the segregation of the chromosome that carries it such that in heterozygous +/t males, the t haplotype is transmitted to >95% of the offspring, a phenomenon known as transmission ratio distortion. The LC2 outer dynein arm light chain of Chlamydomonas reinhardtii is a homologue of the mouse protein Tctex2. We have identified Chlamydomonas insertional mutants with deletions in the gene encoding LC2 and demonstrate that the LC2 gene is the same as the ODA12 gene, the product of which had not been identified previously. Complete deletion of the LC2/ODA12 gene causes loss of all outer arms and a slow jerky swimming phenotype. Transformation of the deletion mutant with the cloned LC2/ODA12 gene restores the outer arms and rescues the motility phenotype. Therefore, LC2 is required for outer arm assembly. The fact that LC2 is an essential subunit of flagellar outer dynein arms allows us to propose a detailed mechanism whereby transmission ratio distortion is explained by the differential binding of mutant (t haplotype encoded) and wild-type dyneins to the axonemal microtubules of t-bearing or wild-type sperm, with resulting differences in their motility.
Rights and Permissions
Citation: Mol Biol Cell. 1999 Oct;10(10):3507-20.