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M F Lyon

Publications and source records attributed to M F Lyon.

At least 109 records · Page 6Linked to original sources
PubMed1983

Evidence for a defective seminiferous tubule barrier in testes of Tfm and Sxr mice.

The competence of the seminiferous tubule barrier was evaluated by determining the sucrose space in isolated testis preparations obtained from adult wild-type mice and from mutants having defects in spermatogenesis. The distribution of [3H]sucrose in testes from wild-type mice was in a space which constituted 18.5% of the [14C]urea space. The corresponding sucrose space in testes from Tfm/Y and Sxr/+ sterile mutants was elevated to 57.7% and 52.0%, respectively. Independent approaches to detect an impairment in the seminiferous tubule barrier of testes from Tfm/Y mice consisted of estimations of the osmotic barrier to hypertonic LiCl, using histological techniques, and determination of the testis sucrose space in vivo. With both approaches, results obtained supported the presence of an impaired barrier in testes of Tfm/Y mice. The sucrose space was within normal limits in testes of the other mutants examined, which were defective in spermatogenesis. The results do not provide any evidence for an impaired barrier in testes of mice having Movbr/Y and Gy/Y mutations, or the t6twl genotype.

Animals↗
PubMed1982

Use of an inversion to test for induced X-linked lethals in mice.

A long X-chromosomal inversion in the mouse was used to suppress crossing-over and thereby to scan 85% of the X-chromosome, or 5% of the genome, for recessive lethal mutations induced by radiation. After a fractionated absorbed dose of 500 + 500 rad X-rays 24 h apart to spermatogonia, 2/536 irradiated and 0/529 control X-chromosomes carried a confirmed lethal. This corresponds to a rate for recessive lethals of 1.9 x 10(-6)/rad/X-chromosome for single exposures (allowing for the enhancing effect of fractionation). This is believed to be the first demonstration of the induction of transmissible X-linked lethals in mammals. The results are consistent with previous findings by other methods and indicate the relatively low rate of induction of lethals and the value of inversions in detecting them.

Animals↗
PubMed1982

Induction of congenital anomalies in offspring of female mice exposed to varying doses of X-rays.

Female mice were exposed to varying absorbed doses (108-504 rad) of X-rays and mated at different intervals after irradiation (1-7, 8-14, 15-21 and 22-28 days). Uterine contents were examined at late pregnancy in order to detect early fetal deaths (dominant lethality) and malformations in the live fetuses. Two trends were apparent from data on abnormal fetuses. At each weekly interval, the incidence of abnormalities tended to rise with increase in dose, and, at any given dose, the incidence tended to increase with time after irradiation. Dwarfism and exencephaly were the two most common malformations found. The changes in incidence of dominant lethality and of abnormal fetuses with time and with dose follow each other closely, the highest incidence for both being reached in week 3 (59 +/- 4.7% for dominant lethals and 12.5 +/- 3.1% for abnormal fetuses, after 504 rad) indicating increased radiosensitivity of less mature oocytes. These results parallel those obtained from known genetic effects reported by other workers and suggest that testing for incidence of congenital malformations among offspring of treated animals may prove a useful means of assessing genetic hazards of radiation or chemicals.

Abnormalities, Radiation-Induced↗
PubMed1980

X-chromosome inactivation in extra-embryonic membranes of diploid parthenogenetic mouse embryos demonstrated by differential staining.

In somatic cells of female mammals one of the two X chromosomes is genetically inactive and heterochromatic, resulting in dosage compensation for X-linked genes. In marsupials the paternally derived X chromosome is preferentially inactivated. In eutherian mammals, although either X chromosome can be inactivated at random in somatic cells, preferential inactivation of the paternally derived X chromosome has been demonstrated cytologically in mouse and rat yolk sac and mouse chorion and biochemically in mouse yolk sac, chorionic ectoderm and trophoblast. In mouse yolk sac the non-random element has been shown both biochemically and cytologically to be confined to the endoderm layer in which there is almost total paternal X-chromosome activity in the separated yolk sac layers of diploid parthenogenetic mouse embryos in which both X chromosomes are maternally derived. Kaufman et al. have demonstrated X inactivation in somatic cells of diploid parthenogenetic embryos, and we have used a modification of Kanda's method, which renders the presumptive inactive X dark staining, to reveal an inactive X chromosome in both endoderm and mesoderm layers of separated yolk sacs from parthenogenones. Thus even in tissues in which there is normally total non-random paternal X inactivation, in the absence of a paternally derived X chromosome a maternally derived X can be inactivated.

Animals↗
PubMed1980

Reduced reproductive performance in androgen-resistant Tfm/Tfm female mice.

Androgen-resistant female mice (Tfm/Tfm) homozygous for the mutant gene Tfm were bred by making use of males chimaeric for the Tfm gene. All seven Tfm/Tfm females found were fertile, confirming that a normal level of androgen receptor protein is not essential for reproduction in female mice. However, when five of the seven were studied throughout their reproductive life they proved to have impaired reproductive performance and premature cessation of reproduction. No impairment of reproduction was seen in heterozygous Tfm/+ females. The ovarian histology suggested that in Tfm/Tfm the normal ageing processes were accelerated. This work is consistent with the work of others in that androgen is involved in the control of follicular maturation and atresia, and that the effect is mediated by the androgen receptor coded by the Tfm locus.

Androgens↗
PubMed1979

t-Haplotypes of the mouse may involve a change in intercalary DNA.

The naturally occurring t-haplotypes of the mouse exhibit a set of peculiar genetic properties, including strong suppression of crossing over in the segment of chromosome 17 between the loci of T and H--2. Study of the genetics of mutant haplotypes suggests that the observed effects on meiosis and embryonic development may be due to an altered form of intercalary DNA (iDNA) in the relevant chromosomal region (band 17B).

Animals↗
PubMed1979

Dose-response curves for radiation-induced gene mutations in mouse oocytes and their interpretation.

Previous work, in which female mice had been given fractionated doses of 20 X 10 rad X-rays, had confirmed and extended Russell's observations that the dose-response relationship for specific-locus mutations in mature-mouse oocytes is curved at low doses. The present work was intended to study the relationship at relatively high doses. Adult female mice were given doses of 200, 400 or 600 rad x-rays at 52 or 72 rad/min, and mated immediately. Offspring conceived in the first 7 days (i.e. using oocytes which were mature at time of treatment) were scored for specific-locus mutations. The data indicate that the departure from linearity of the dose-response curve is marginally significant at the 5% level. A quadratic dose-response curve (y = c + aD + bD2) and a square-law relationship (y = c + bD2) both give a good fit to the data. Both curves fit data of other authors obtained at low doses or dose-rates. These results could be interpreted either in terms of dose-dependent repair phenomena, or by considering specific-locus mutations as two-track events. In view of knowledge of other phenomena concerning mutation and cell killing in mouse oocytes, such as the variation in sensitivity of different cell stages, the interpretation in terms of repair phenomena is preferred.

Animals↗
PubMed1979

Reproductive capacity and dominant lethal mutations in female guinea-pigs and Djungarian hamsters following X-rays or chemical mutagens.

The reproductive capacity and induction of dominant lethal mutations in adult female guinea-pigs and Djungarian hamsters were tested following treatment with 400 rad X-rays, 1.6 mg/kg triethylenemelamine (TEM) or 75 mg/kg isopropylmethanesulphonate (IPMS). A fairly high level of dominant lethals were observed in female guinea-pigs mated at the first oestrus after irradiation (23.4 +/- 6.4%) with a lower yield at 3 months (9.6 +/- 8.2%). Neither of the chemicals caused any significant induction of dominant lethals at either mating time. In the reproductive capacity experiments, the mean litter size of irradiated female guinea-pigs was reduced for about 12 months and this was especially marked in the first 6 months following treatment. Neither of the chemicals caused any significant differences in early litter sizes but there was a noticeable reduction in the litter sizes of TEM-treated females in the 18--24 month interval. With Djungarian hamsters a marked effect of X-rays on reproductive capacity was apparent. After 400 rad a smaller proportion of irradiated females littered in the first 25-day interval than after the other treatments, and no irradiated females produced more than one litter. Neither of the chemicals caused such a drastic reduction in fertility but TEM-treated females produced fewer litters and became sterile at an earlier age than control or IPMS-treated females. With IPMS, the number of litters produced was similar to the controls. Both chemicals caused a significant reduction in litter-size but further work is needed to establish whether this was due to induction of dominant lethals. No translocations were observed in the sons of treated female guinea-pigs or hamsters, but the numbers of animals studied were too small for any conclusions to be drawn.

Animals↗