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

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.

1991 ◽  
Vol 57 (2) ◽  
pp. 153-157 ◽  
Author(s):  
William Garside ◽  
Christine Ruangvoravat ◽  
Patricia Dolan ◽  
Nina Hillman

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.


1989 ◽  
Vol 53 (1) ◽  
pp. 25-28 ◽  
Author(s):  
William Garside ◽  
Nina Hillman

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.


1989 ◽  
Vol 54 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Lee M. Silver

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.


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 ◽  
...  

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

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.


Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 785-792
Author(s):  
U Kevin Ewulonu ◽  
Kerry Schimenti ◽  
Barbara Kuemerle ◽  
Terry Magnuson ◽  
John Schimenti

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.


Genetics ◽  
1986 ◽  
Vol 114 (1) ◽  
pp. 235-245
Author(s):  
Gregory R Gummere ◽  
Paulette J McCormick ◽  
Dorothea Bennett

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.


2018 ◽  
Vol 29 (6) ◽  
pp. 751-762 ◽  
Author(s):  
Shengya Cao ◽  
Keda Zhou ◽  
Zhening Zhang ◽  
Karolin Luger ◽  
Aaron F. Straight

Eukaryotic centromeres are defined by the presence of nucleosomes containing the histone H3 variant, centromere protein A (CENP-A). Once incorporated at centromeres, CENP-A nucleosomes are remarkably stable, exhibiting no detectable loss or exchange over many cell cycles. It is currently unclear whether this stability is an intrinsic property of CENP-A containing chromatin or whether it arises from proteins that specifically associate with CENP-A chromatin. Two proteins, CENP-C and CENP-N, are known to bind CENP-A human nucleosomes directly. Here we test the hypothesis that CENP-C or CENP-N stabilize CENP-A nucleosomes in vitro and in living cells. We show that CENP-N stabilizes CENP-A nucleosomes alone and additively with CENP-C in vitro. However, removal of CENP-C and CENP-N from cells, or mutating CENP-A so that it no longer interacts with CENP-C or CENP-N, had no effect on centromeric CENP-A stability in vivo. Thus, the stability of CENP-A nucleosomes in chromatin does not arise solely from its interactions with CENP-C or CENP-N.


1993 ◽  
Vol 62 (2) ◽  
pp. 133-137 ◽  
Author(s):  
Lee M. Silver ◽  
Christine Buck

SummaryA novel central partial t haplotype was generated by screening for a recombination event between overlapping distal and proximal partial haplotypes. This haplotype contains just two elements Tcrt and Tcd-3t —involved in the t-specific transmission ratio distortion phenotype. Breeding analysis of males that carry this chromosome provides evidence that Tcd-3 is, indeed, a distorter locus and not a second responder. Furthermore, the data indicate that a single well-defined distorter locus is insufficient to overcome completely the self-destructive, low transmission ratio distortion phenotype expressed by the t allele at the t complex responder locus, although a small, but highly significant, effect was observed.


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