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dc.contributor.authorPazour, Gregory J.
dc.contributor.authorKoutoulis, Anthony
dc.contributor.authorBenashski, Sharon E.
dc.contributor.authorDickert, Bethany L.
dc.contributor.authorSheng, Hong
dc.contributor.authorPatel-King, Ramila S.
dc.contributor.authorKing, Stephen M.
dc.contributor.authorWitman, George B.
dc.date2022-08-11T08:09:33.000
dc.date.accessioned2022-08-23T16:35:19Z
dc.date.available2022-08-23T16:35:19Z
dc.date.issued1999-10-08
dc.date.submitted2009-03-24
dc.identifier.citationMol Biol Cell. 1999 Oct;10(10):3507-20.
dc.identifier.issn1059-1524 (Print)
dc.identifier.pmid10512883
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38531
dc.description.abstractTctex2 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10512883&dopt=Abstract">Link to Article in PubMed</a>
dc.subjectAnimals
dc.subjectCell Movement
dc.subjectChlamydomonas reinhardtii
dc.subjectCloning, Molecular
dc.subjectDynein ATPase
dc.subjectFlagella
dc.subject*Genes, Protozoan
dc.subject*Intracellular Signaling Peptides and Proteins
dc.subjectMice
dc.subjectMicroscopy, Electron
dc.subject*Microtubule-Associated Proteins
dc.subjectMicrotubules
dc.subjectMutation
dc.subjectNuclear Proteins
dc.subjectPhenotype
dc.subjectProtozoan Proteins
dc.subjectSequence Homology
dc.subjectTransformation, Genetic
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleLC2, the chlamydomonas homologue of the t complex-encoded protein Tctex2, is essential for outer dynein arm assembly
dc.typeJournal Article
dc.source.journaltitleMolecular biology of the cell
dc.source.volume10
dc.source.issue10
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2400&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1401
dc.identifier.contextkey794898
refterms.dateFOA2022-08-23T16:35:19Z
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/1401
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages3507-20


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