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 Deletion of mouse t-complex distorter-1 produces an effect like that of the t-form of the distorter

1992 ◽  
Vol 59 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Sterility ◽  
Differential Susceptibility ◽  
Proximal Part ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
T Complex ◽  
Severe Impairment ◽  
Ratio Distortion ◽  
Distorter Gene

SummaryAn allele of the mouse brachyury locus, T22H, had been shown previously to involve a deletion of several markers in the proximal part of chromosome 17, and almost certainly includes deletion of the t-complex distorter gene Tcd-1. The effects of T22H on transmission ratio distortion and male sterility caused by the t-complex were compared with those of a partial t-haplotype th51, which carries the t-form of the distorter Tcd-1t. In combination with the complete haplotypetf32, T22H caused severe impairment of male fertility, but males of genotype T22H/t6 or T22H/thSl were normally fertile. These results were very similar to those obtained when th51 was in combination with the same haplotypes. In effect on transmission ratio T22H was again similar to thSI, in that it produced a marked increase in the transmission of the haplotype t6. To test whether the effects of T22H were due to deletion of elements other than Tcd-1, the effect of T22H on transmission of the partial haplotype th2 was compared with that of the deletion Thv. Again T22H markedly increased transmission of the t-haplotype and the effect was significantly greater than the small effect produced by Thp.It is concluded that deletion of the distorter Tcd-1 has an effect like that of the t-form of this distorter, Tcd-1t, and hence that Ted-11 must be an amorph or hypomorph. It is speculated that other t-complex distorters, Tcd-2t and Tcd-3t may also be amorphs or hypomorphs. Thus, the phenomena of transmission ratio distortion and male sterility due to the t-complex appear to be brought about by differential susceptibility of wild-type and t-responder alleles, Tcr+ and Tcrt, to a shortage of distorter gene product.

scholarly journals Gene dosage effects on transmission ratio distortion and fertility in mice that carry t haplotypes

1989 ◽  
Vol 54 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Lee M. Silver
Keyword(s):  
Gene Dosage ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Double Dose ◽  
Absolute Level ◽  
T Complex ◽  
Gene Dosage Effects ◽  
Ratio Distortion ◽  
The Individual ◽  
Very High

SummaryComplete t haplotypes can be transmitted at distorted ratios from heterozygous +/t male mice as a consequence of t-specific alleles at a series of t complex distorter loci (Tcd-1t through Tcd-4t) and a t complex responder locus. Partial t haplotypes that lack the Tcd-2t allele cannot be transmitted at the very high ratios characteristic of complete t haplotypes. The breeding studies reported here tested the possibility that the absence of Tcd-2t could be compensated for by the presence of double doses of other Tcdt alleles. The results indicate that a double dose of Tcd-4t alone will not work, but that a double dose of both Tcd-1t and Tcd-4t can promote a very high transmission ratio in the absence of Tcd-2t. These results suggest that the extent to which transmission ratios are distorted is dependent upon the absolute level of expression of the individual Tcd genes. Further studies of genotypic effects on transmission ratio distortion, as well as fertility, lead to the suggestion of a fifth t complex distorter (Tcd-5) locus within t haplotypes.

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.

A premature acrosome reaction is programmed by mouse t haplotypes during sperm differentiation and could play a role in transmission ratio distortion

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 769-773 ◽  
Author(s):  
J. Brown ◽  
J.A. Cebra-Thomas ◽  
J.D. Bleil ◽  
P.M. Wassarman ◽  
L.M. Silver
Keyword(s):  
Acrosome Reaction ◽  
Genetic Data ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Relative Advantage ◽  
Transmission Ratio ◽  
Ratio Distortion ◽  
Sperm Dysfunction

Mouse t haplotypes are variant forms of chromosome 17 that can be transmitted at non-Mendelian ratios by heterozygous +/t males. The accumulated genetic data indicate that ‘+-sperm’ and ‘t-sperm’ are produced in equal numbers but that most ‘+-sperm’ are rendered dysfunctional, so that ‘t-sperm’ have a relative advantage at fertilization. To date, the basis for this t-induced sperm dysfunction has remained unknown. Here we demonstrate that a high proportion of sperm obtained from certain strains of +/t mice undergo a premature acrosome reaction under in vitro capacitation conditions. The simplest interpretation of these data, in conjunction with previous results, is that developing ‘+-spermatids’ are preprogrammed by ‘t-spermatids’ to undergo this premature reaction. Since acrosome-reacted sperm are unable to participate in the process of fertilization, this defect could account for the extreme distortion of transmission ratio observed from mice heterozygous for a class of complete t haplotypes.

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 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.

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