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Vol. 10, Issue 10, 3507-3520, October 1999



and
*Department of Cell Biology, University of Massachusetts Medical
School, Worcester, Massachusetts 01655; 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.
Cell Biology
Group, School of Plant Science, The University of Tasmania, Hobart,
Tasmania 7001 Australia; and
Department of Biochemistry,
University of Connecticut Health Center, Farmington, Connecticut
06030-3305
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