scholarly journals LC2, the Chlamydomonas Homologue of the tComplex-encoded Protein Tctex2, Is Essential for Outer Dynein Arm Assembly

1999 ◽  
Vol 10 (10) ◽  
pp. 3507-3520 ◽  
Author(s):  
Gregory J. Pazour ◽  
Anthony Koutoulis ◽  
Sharon E. Benashski ◽  
Bethany L. Dickert ◽  
Hong Sheng ◽  
...  
Keyword(s):  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Wild Type ◽  
Gene Encoding ◽  
Ratio Distortion ◽  
Differential Binding ◽  
Phenotype Transformation ◽  
Essential Subunit ◽  
Complete Deletion ◽  
T Haplotype

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.

Concerted evolution of the mouse Tcp-10 gene family: Implications for the functional basis of t haplotype transmission ratio distortion

Genomics ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Stephen H. Pilder ◽  
Cindy L. Decker ◽  
Salim Islam ◽  
Christine Buck ◽  
Judith A. Cebra-Thomas ◽  
...  
Keyword(s):  
Gene Family ◽  
Concerted Evolution ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Functional Basis ◽  
Ratio Distortion ◽  
T Haplotype

scholarly journals Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

1998 ◽  
Vol 71 (2) ◽  
pp. 119-125 ◽  
Author(s):  
DIETER WEICHENHAN ◽  
BÄRBEL KUNZE ◽  
WALTHER TRAUT ◽  
HEINZ WINKING
Keyword(s):  
Transmission Ratio Distortion ◽  
Chromosome 1 ◽  
Transmission Ratio ◽  
Recovery Ratio ◽  
Wild Type ◽  
Variable Cluster ◽  
Ratio Distortion ◽  
Normal Transmission ◽  
Mendelian Transmission ◽  
Mouse Chromosome 1

The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUTdel, shows normal transmission ratios and no compensating capability. In this respect, MUTdel behaves like a wild-type cluster. Hence, both properties – transmission ratio distortion and compensating capability – map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.

scholarly journals Deletion analysis of male sterility effects of t–haplotypes in the mouse

1990 ◽  
Vol 56 (2-3) ◽  
pp. 179-183 ◽  
Author(s):  
Dorothea Bennett ◽  
Karen Artzt
Keyword(s):  
Male Sterility ◽  
Deletion Analysis ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Wild Type ◽  
Ratio Distortion ◽  
Very High

SummaryWe present data on the effects of three chromosome 17 deletions on transmission ratio distortion (TRD) and sterility of several t-haplotypes. All three deletions have similar effects on male TRD: that is, Tdel/tcomplete genotypes all transmit their t–haplotype in very high proportion. However, each deletion has different effects on sterility of heterozygous males, with Tor/t being fertile, Thp/t less fertile, and Torl/t still less fertile. These data suggest that wild-type genes on chromosomes homologous to f-haplotypes can be important regulators of both TRD and fertility in males, and that the wild-type genes concerned with TRD and fertility are at least to some extent different. The data also provide a rough map of the positions of these genes.

scholarly journals Targeted Mutagenesis of a Candidate t Complex Responder Gene in Mouse t Haplotypes Does Not Eliminate Transmission Ratio Distortion

Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 785-792
Author(s):  
U Kevin Ewulonu ◽  
Kerry Schimenti ◽  
Barbara Kuemerle ◽  
Terry Magnuson ◽  
John Schimenti
Keyword(s):  
Es Cells ◽  
Targeted Mutagenesis ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Functional Assay ◽  
T Complex ◽  
Actual Nature ◽  
Splicing Pattern ◽  
Ratio Distortion ◽  
T Haplotype

Abstract Transmission ratio distortion (TRD) associated with mouse t haplotypes causes +/t males to transmit the t-bearing chromosome to nearly all their offspring. Of the several genes involved in this phenomenon, the t complex responder (Tcrt) locus is absolutely essential for TRD to occur. A candidate Tcrt gene called Tcpl0bt was previously cloned from the genetically defined Tcrt region. Its location, restricted expression in testis, and a unique postmeiotic alternative splicing pattern supported the idea that Tcp10bt was Tcrt. To test this hypothesis in a functional assay, ES cells were derived from a viable partial t haplotype, and the Tcp10bt gene was mutated by homologous recombination. Mutant mice were mated to appropriate partial t haplotypes to determine whether the targeted chromosome exhibited transmission ratios characteristic of the responder. The results demonstrated that the targeted chromosome retained full responder activity. Hence, Tcp10bt does not appear to be Tcrt. These and other observations necessitate a reevaluation of genetic mapping data and the actual nature of the responder.

scholarly journals Transmission Ratio Distortion Due to the bl Gene in Table Beet

2001 ◽  
Vol 126 (3) ◽  
pp. 340-343 ◽  
Author(s):  
Diane Austin ◽  
I.L. Goldman
Keyword(s):  
Single Gene ◽  
Recessive Gene ◽  
Segregation Ratio ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Wild Type ◽  
Gene Model ◽  
Male Gametes ◽  
Ratio Distortion ◽  
The Individual

The bl gene conditions a blotchy phenotype (irregular sectors of red and white root color) in table beet (Beta vulgaris ssp. vulgaris). Segregation of the bl gene was found to be consistent with a single recessive gene, however, some evidence for a departure from a single gene model was observed when blbl plants were used as females. In this report, segregation of the bl gene was examined in greater detail in 10 F2 populations derived from crosses of red blotchy-rooted females (genotype blbl, denoted blotchy) with red-rooted males (BlBl, denoted red,), and 10 F2 populations derived from the reciprocal cross. In blbl × BlBl crosses, the proportion of red-rooted progeny was greater than 0.75 in seven of the crosses, and was significantly greater (P = 0.005) in three crosses. A test for heterogeneity was significant, indicating that the proportion of red-rooted progeny differed significantly in these 10 crosses. In BlBl × blbl crosses, the proportion of red-rooted progeny was <0.75 in seven of the crosses and there were no significant departures from the expected 3:1 ratio in any of the individual crosses. However, a pooled estimate of the segregation ratio showed a significant (P < 0.01) departure from the 3:1 ratio (pooled estimate = 0.71). These data demonstrate transmission ratio distortion at the bl locus when blbl plants are used as both females and males in matings with wild type plants, but the degree of distortion is greater when blbl plants are used as females. Ratio distortion in such crosses may be due to a variety of factors, including increased transmission of the bl gene through female or male gametes depending on the direction of the cross, reduced fitness of maternally derived blbl progeny, epigenetic phenomena, increased fitness of paternally derived blbl progeny, or linkage of the bl gene to viability genes.

scholarly journals THE INFLUENCE OF GENETIC BACKGROUND AND THE HOMOLOGOUS CHROMOSOME 17 ON t-HAPLOTYPE TRANSMISSION RATIO DISTORTION IN MICE

Genetics ◽  
1986 ◽  
Vol 114 (1) ◽  
pp. 235-245
Author(s):  
Gregory R Gummere ◽  
Paulette J McCormick ◽  
Dorothea Bennett
Keyword(s):  
Genetic Background ◽  
Homologous Chromosome ◽  
Intrinsic Property ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Quantitative Character ◽  
Congenic Lines ◽  
Ratio Distortion ◽  
T Haplotype

ABSTRACT Transmission ratio distortion is a characteristic of complete t-haplotypes, such that heterozygous males preferentially transmit the t-haplotype bearing chromosome 17 to the majority of their progeny. At least two genes contained within the t-haplotype have been identified as being required for such high transmission ratios. In this study we examine the effects of the genetic background and the chromosome homologous to the t-haplotype on transmission ratio distortion. We use two different congenic lines: (1) BTBRTF/Nev.Ttf/t12, in which the t12 haplotype has a transmission ratio of 52%, and (2) C3H/DiSn.Ttf/t12, in which the t12 haplotype has a transmission ratio of 99%. By intercrossing these two strains to produce reciprocal F1 and F2 generations, we have isolated the effects of the homologous chromosome 17 from the effects of the genetic background. We demonstrate that both the homologous chromosome and the genetic background have profound effects on t-haplotype transmission ratio distortion. Furthermore, it is evident that the t-haplotype transmission ratio behaves as a quantitative character rather than an intrinsic property of t-haplotypes.

scholarly journals A structural gene (Tcp-1) within the mouse t complex is separable from effects on tail length and lethality but may be associated with effects on spermatogenesis

1981 ◽  
Vol 38 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Lee M. Silver
Keyword(s):  
Genetic Basis ◽  
Genetic Factors ◽  
Tail Length ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Cell Protein ◽  
Wild Type ◽  
T Complex ◽  
Interaction Factor ◽  
Ratio Distortion

SUMMARYThe Tcp-1 gene is located within the t complex and codes for a major testicular cell protein called p63/6.9. All wild-type chromosomes carry the Tcp-1b allele which codes for a basic form of this protein, while all complete t haplotypes carry the Tcp-1a allele which codes for an acidic form of this protein. It is not clear whether the Tcp-1 gene is associated with phenotypic effects of t haplotypes on embryogenesis and/or spermatogenesis, since the genetic basis for these effects is extremely complex. The elegant analysis of Lyon & Mason (1977) has allowed the identification and separation of a family of genetic factors which interact to produce the observed phenotypes associated with various combinations of t haplotypes. The data summarized in this report indicate that the Tcp-1a locus is separable from all of the identified t haplotype factors except for one; a complete correlation has been obtained between Tcp-1a and a proximal t haplotype factor which is involved in effects on transmission ratio distortion. Two other novel points emerge from this analysis. First, it appears that the tail interaction factor and the proximal sperm factors represent distinct genetic loci. Second, the accumulated data lead to the proposal that the TOrl chromosome carries a short segment of t haplotype chromatin containing Tcp-1a and proximal sperm factors involved in transmission ratio distortion and sterility.

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