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 The in vivo and in vitro transmission ratio distortion of one complete and two partial t haplotypes in mice

1991 ◽  
Vol 57 (2) ◽  
pp. 153-157 ◽  
Author(s):  
William Garside ◽  
Christine Ruangvoravat ◽  
Patricia Dolan ◽  
Nina Hillman
Keyword(s):  
Genetic Model ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Different Types ◽  
Ratio Distortion

SummaryThe effects of different types of insemination (normal and delayed matings and in vitro fertilization) on the transmission ratio distortion (TRD) of three t haplotypes were determined. The tw73 haplotype which contains all of the loci known to affect TRD is transmitted at equivalent frequencies in normal matings and in in vitro fertilizations (0·84 and 0·85, respectively) but at a significantly lower frequency (0·62) in delayed matings. The distal partial th18 haplotype is transmitted at equivalent frequencies in all types of insemination (0·66 to 0·70) while the proximal partial tw18 haplotype is transmitted in Mendelian frequencies in normal matings and in in vitro inseminations but at a significantly lower frequency in delayed matings. The results are discussed with reference to the current genetic model for transmission ratio distortion.

Transmission ratio distortion at the growth hormone gene (GH1) in bovine preimplantation embryos: An in vitro culture-induced phenomenon?

2008 ◽  
Vol 75 (5) ◽  
pp. 715-722 ◽  
Author(s):  
Angela M. Murphy ◽  
Kieran G. Meade ◽  
Patricia A. Hayes ◽  
Stephen D.E. Park ◽  
Alex C.O. Evans ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Vitro Culture ◽  
Transmission Ratio Distortion ◽  
Preimplantation Embryos ◽  
Transmission Ratio ◽  
Growth Hormone Gene ◽  
Ratio Distortion

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 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 Mendelian inheritance of t haplotypes in house mouse (Mus musculus domesticus) field populations

2008 ◽  
Vol 90 (4) ◽  
pp. 331-339 ◽  
Author(s):  
ANN EILEEN MILLER BAKER
Keyword(s):  
House Mouse ◽  
Mus Musculus ◽  
Mendelian Inheritance ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Mus Musculus Domesticus ◽  
Selfish Dna ◽  
Ratio Distortion ◽  
Deleterious Genes

SummaryAlleles of many genes in the house mouse (Mus musculus domesticus) t complex influence embryonic development, male transmission ratio, male fertility and other traits. Homozygous t lethal alleles cause prenatal lethality, whereas male t semilethal homozygotes and males heterozygous for two complementing t lethal haplotypes are sterile. Without a mechanism maintaining these deleterious genes, t lethals and t semilethals should be eliminated by selection. The mechanism for maintaining them is transmission ratio distortion (TRD), which is said to occur when a t/+ male sires a significantly greater proportion of fetuses carrying his t haplotype (80–100%) than his wild-type chromosome 17. To understand how this selfish DNA functions in trapped populations, the objectives of this study were to examine the structure of t haplotypes in Colorado field populations and to determine transmission ratios in these populations. The data presented here indicate two possible causes for lower than expected transmission ratios in field populations: (1) single-sire fertilization by sperm from mosaic t males may lack all t haplotype genes causing high TRD. (2) t-bearing sperm fertilizing multiple-sire litters are diluted by+sperm from males having the most common genotype (+/+).

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.

Quantitation of two-dimensional gel proteins reveals unequal amounts of Tcp-1 gene products during mouse spermatogenesis but no correlation with transmission ratio distortion

Development ◽  
1985 ◽  
Vol 89 (1) ◽  
pp. 123-131
Author(s):  
Edwin R. Sánchez ◽  
Craig Hammerberg ◽  
Robert P. Erickson
Keyword(s):  
Protein A ◽  
Intrinsic Property ◽  
Transmission Ratio Distortion ◽  
Molecular Probe ◽  
Transmission Ratio ◽  
T Complex ◽  
In Vivo Labelling ◽  
Ratio Distortion

The discovery of a protein, p63/6·9, that is synthesized by both somatic and germ cells and coded for by a gene, Tcp-1, within the t complex provides a molecular probe for examining transmission ratio distortion in t mice. Two electromorphs of this protein exist. The acidic protein (a) is encoded by t-haplotype chromosomes, while the basic protein (b) is encoded by wild-type 17th chromosomes. We have measured the relative amounts of p63/6·9a and p63/6·9b for various t-complex bearing males and for several stages of spermatogenesis. There was no correlation between the ratio of p63/6·9a to b and the magnitude of transmission ratio distortion but the relative amounts of these proteins present in testicular cells can vary depending on the method of labelling. In vivo labelling results in the detection of two-fold greater amounts of p63/6·9a while in vitro labelling produces equimolar amounts of these two proteins. These data suggest that unequal synthesis or degradation of the p63/6·9 proteins occurs during spermatogenesis. It is proposed that increased synthesis of p63/6·9a in vivo is an intrinsic property of t-haplotypes.

scholarly journals The transmission ratio distortion of the th2-haplotype in vivo and in vitro

1989 ◽  
Vol 53 (1) ◽  
pp. 25-28 ◽  
Author(s):  
William Garside ◽  
Nina Hillman
Keyword(s):  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Low Frequencies ◽  
Transmission Frequency ◽  
Ratio Distortion

SummaryThe th2-haplotype is transmitted at low frequencies (< 0·30) by + / th2 males in normal matings. In the studies described here, the transmission frequency of the th2-haplotype from Rb7 / th2 males was determined for normal and delayed matings and in vitro inseminations. The data show the transmission frequency from the two in vivo inseminations to be less than 0·30 and to be statistically equivalent. However, the in vitro transmission frequency (0·80) is significantly greater than either of the in vivo frequencies. The results show that the environment in which fertilization occurs affects the transmission frequency of this specific t-haplotype significantly.

scholarly journals Narrowing the Critical Regions for Mouse t Complex Transmission Ratio Distortion Factors by Use of Deletions

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 793-801 ◽  
Author(s):  
Mary F Lyon ◽  
John C Schimenti ◽  
Edward P Evans
Keyword(s):  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Critical Interval ◽  
Enhanced Transmission ◽  
T Complex ◽  
Ratio Distortion ◽  
Critical Regions ◽  
Complex Transmission ◽  
T Haplotype

Abstract Previously a deletion in mouse chromosome 17, T22H, was shown to behave like a t allele of the t complex distorter gene Tcd1, and this was attributed to deletion of this locus. Seven further deletions are studied here, with the aim of narrowing the critical region in which Tcd1 must lie. One deletion, T30H, together with three others, T31H, T33H, and T36H, which extended more proximally, caused male sterility when heterozygous with a complete t haplotype and also enhanced transmission ratio of the partial t haplotype t 6, and this was attributed to deletion of the Tcd1 locus. The deletions T29H, T32H, and T34H that extended less proximally than T30H permitted male fertility when opposite a complete t haplotype. These results enabled narrowing of the critical interval for Tcd1 to between the markers D17Mit164 and D17Leh48. In addition, T29H and T32H enhanced the transmission ratio of t6, but significantly less so than T30H. T34H had no effect on transmission ratio. These results could be explained by a new distorter located between the breakpoints of T29H and T34H (between T and D17Leh66E). It is suggested that the original distorter Tcd1 in fact consists of two loci: Tcd1a, lying between D17Mit164 and D17Leh48, and Tcd1b, lying between T and D17Leh66E.

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