In:
Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 10, No. 10 ( 1999-10), p. 3507-3520
Abstract:
Tctex2 is thought to be one of the distorter genes of the mouset 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 ofChlamydomonas reinhardtii is a homologue of the mouse protein Tctex2. We have identified Chlamydomonasinsertional 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 oft-bearing or wild-type sperm, with resulting differences in their motility.
Type of Medium:
Online Resource
ISSN:
1059-1524
,
1939-4586
DOI:
10.1091/mbc.10.10.3507
Language:
English
Publisher:
American Society for Cell Biology (ASCB)
Publication Date:
1999
detail.hit.zdb_id:
1474922-1
SSG:
12