scholarly journals Differences in or near the responder region of complete and partial mouse t-haplotypes

1987 ◽  
Vol 50 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Mary F. Lyon ◽  
Joanna Zenthon
Keyword(s):  
Harmful Effect ◽  
Complex Form ◽  
Transmission Ratio Distortion ◽  
Wild Type ◽  
Homologous Chromosomes ◽  
Cis Acting ◽  
Ratio Distortion ◽  
Lower Transmission ◽  
In Cis ◽  
Harmful Effects

SummaryThe transmission ratio distortion seen in males heterozygous for a mouse t-complex has been explained on the basis of trans-acting distorter genes, having a harmful effect on a responder gene. The t-complex form of the responder is relatively resistant to these harmful effects and hence is preferentially transmitted. Animals homozygous for the t-complex responder would be expected to show equal transmission of the two homologous chromosomes, but this is not always so. Studies described in this paper have shown differences among complete t's in their transmission when opposite a constant responder carrying partial t-haplotype. In addition, the proximal partial haplotypes th49 and tw18, both derived from tw5 but of different lengths, behave differently when opposite a responder. The three central partial haplotypes, tlowH, tlow2H and tlow3H, also differ, in that tlow3H shows lower transmission than tlowH or tloW2H when opposite either wild-type, or another responder, or distorter genes. These results can be explained either on the basis of differences in the responder region of various haplotypes, including the possibility of varying numbers of copies of the relevant sequences, or on the basis of differences in cis-acting (as opposed to trans-acting) distorter genes.

scholarly journals Search for differences among t haplotypes in distorter and responder genes

1990 ◽  
Vol 55 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Genetic Background ◽  
Complex Form ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Naturally Occurring ◽  
Harmful Action ◽  
Ratio Distortion ◽  
Harmful Effects

SummaryTransmission ratio distortion due to the mouse t complex is thought to be due to harmful effects of trans-acting distorter genes acting on a responder, with the t complex form of the responder being relatively resistant to this harmful action of the distorters. Previous work had indicated that naturally occurring t haplotypes differed in their responders or in distorters lying near the responder, with the result that animals doubly heterozygous for two responder-carrying haplotypes transmitted these haplotypes unequally. In the present work t haplotypes could be divided into three types on the basis of their transmission when doubly heterozygous with the responder-carrying partial haplotype tlowH. The majority, t0, t6, tw1, tw2 and tw73, were transmitted equally with tlowH, a second group, including tw5 and two haplotypes derived from it, were transmitted less frequently than tlowH, and the single member of a third group, t32, was transmitted in excess of tlowH This last result suggests that the underlying differences are in the responder itself, rather than in the distorters. Search for differences among t haplotypes in distorters produced some equivocal results possibly resulting from effects of genetic background. In particular, results of others suggesting presence of a fourth distorter, Tcd-4, were not confirmed.

scholarly journals Distorter genes of the mouse t-complex impair male fertility when heterozygous

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Fertility ◽  
Genetic Background ◽  
Inbred Strains ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Male Mice ◽  
Wild Type ◽  
T Complex ◽  
Ratio Distortion ◽  
Harmful Effects

SummaryMale mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

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.

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 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 A Chlamydomonas Homologue of the Putative Murine t Complex Distorter Tctex-2 Is an Outer Arm Dynein Light Chain

1997 ◽  
Vol 137 (5) ◽  
pp. 1081-1090 ◽  
Author(s):  
Ramila S. Patel-King ◽  
Sharon E. Benashski ◽  
Alistair Harrison ◽  
Stephen M. King
Keyword(s):  
Molecular Analysis ◽  
Light Chain ◽  
Meiotic Drive ◽  
Cytoplasmic Dynein ◽  
Transmission Ratio Distortion ◽  
Dynein Light Chain ◽  
Wild Type ◽  
Biochemical Model ◽  
T Complex ◽  
Ratio Distortion

Molecular analysis of a 19,000-Mr protein from the Chlamydomonas flagellum reveals that it is homologous to the t complex–encoded protein Tctex-2, which is a candidate for one of the distorter products that cause the extreme transmission ratio distortion (meiotic drive) of the murine t complex. The 19,000-Mr protein is extracted from the axoneme with 0.6 M NaCl and comigrates with the outer dynein arm in sucrose density gradients. This protein also is specifically missing in axonemes prepared from a mutant that does not assemble the outer arm. These data raise the possibility that Tctex-2 is a sperm flagellar dynein component. Combined with the recent identification of Tctex-1 (another distorter candidate) as a light chain of cytoplasmic dynein, these results lead to a biochemical model for how differential defects in spermiogenesis that result in the phenomenon of meiotic drive might be generated in wild-type vs t-bearing sperm.

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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