Oocyte heterogeneity with respect to the meiotic silencing of unsynapsed X chromosomes in the XY female mouse

Oocytes with adhering follicle cells were sampled from ovaries obtained from 11 GPI-1A—GPI-1B chimaeras, comprising 10 females and 1 hermaphrodite. GPI analysis of individual oocytes revealed a marked bias towards the GPI-1B component in the germ line of this chimaeric combination. GPI-1B XY oocytes were identified in the ovary from the hermaphrodite, the bias towards the GPI-1B germ line perhaps helping to counterbalance the normally severe selection against XY oocytes. GPI analysis of follicle cells revealed a much more balanced contribution of the two components to this ovarian cell type. Importantly, GPI-1A follicle cells were identified in more than half the follicles from an XX—XY female in which the GPI-1A component was XY, supporting an earlier conclusion of Ford et al. (1974) that XY cells can contribute to the follicles of XX—XY female mice. It is suggested that XY cells can be recruited to form follicle cells in XX—XY chimaeras when there is a developmental mismatch between the two components, such that an ovary-determining signal produced by the XX component pre-empts the testis-determining action of the Y.

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Premature ovarian insufficiency in the XO female mouse on the C57BL/6J genetic background

MHR Basic science of reproductive medicine ◽

10.1093/molehr/gaaa049 ◽

2020 ◽

Vol 26 (9) ◽

pp. 678-688

Author(s):

B Vaz ◽

F El Mansouri ◽

X Liu ◽

T Taketo

Keyword(s):

Female Mouse ◽

Genetic Background ◽

Congenital Abnormalities ◽

Ovarian Insufficiency ◽

Female Progeny ◽

X Chromosomes ◽

Monosomy X ◽

Physical Defects ◽

Female Germline ◽

The Impact

Abstract In humans, all but 1% of monosomy 45.X embryos die in utero and those who reach term suffer from congenital abnormalities and infertility termed Turner’s syndrome (TS). By contrast, XO female mice on various genetic backgrounds show much milder physical defects and normal fertility, diminishing their value as an animal model for studying the infertility of TS patients. In this article, we report that XO mice on the C57BL/6J (B6) genetic background showed early oocyte loss, infertility or subfertility and high embryonic lethality, suggesting that the effect of monosomy X in the female germline may be shared between mice and humans. First, we generated XO mice on either a mixed N2(C3H.B6) or B6 genetic background and compared the number of oocytes in neonatal ovaries; N2.XO females retained 45% of the number of oocytes in N2.XX females, whereas B6.XO females retained only 15% of that in B6.XX females. Second, while N2.XO females were as fertile as N2.XX females, both the frequency of delivery and the total number of pups delivered by B6.XO females were significantly lower than those by B6.XX females. Third, after mating with B6 males, both N2.XO and B6.XO females rarely produced XO pups carrying paternal X chromosomes, although a larger percentage of embryos was found to be XO before implantation. Furthermore, B6.XO females delivered 20% XO pups among female progeny after mating with C3H males. We conclude that the impact of monosomy X on female mouse fertility depends on the genetic background.

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Evidence of non-random X chromosome activity in the mouse

Genetics Research ◽

10.1017/s001667230001449x ◽

1972 ◽

Vol 19 (3) ◽

pp. 229-240 ◽

Cited By ~ 61

Author(s):

B. M. Cattanach ◽

C. E. Williams

Keyword(s):

X Chromosome ◽

Female Mouse ◽

Somatic Cells ◽

Inbred Strains ◽

X Inactivation ◽

Cell Populations ◽

Alternative States ◽

X Chromosomes ◽

Inbred Strains Of Mice ◽

Controlling Element

SUMMARYX-linked modification of the heterozygous phenotypes of X-linked genes has been detected in the X chromosomes of several inbred strains of mice. The effect is similar to that of the alternative ‘states’ or alleles, of the X chromosome controlling element, Xce, identified in T(1; X)Ct X chromosomes. Tests on two such differing X chromosomes have indicated that the phenotypic modification results either from non-random inactivation of the two X chromosomes or from selection operating on the two cell populations differentiated by X-inactivation. The data provide evidence of non-random X chromosome activity in the somatic cells of the female mouse.

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Both X chromosomes function before visible X-chromosome inactivation in female mouse embryos

Nature ◽

10.1038/274500a0 ◽

1978 ◽

Vol 274 (5670) ◽

pp. 500-503 ◽

Cited By ~ 141

Author(s):

CHARLES J. EPSTEIN ◽

SANDRA SMITH ◽

BRUCE TRAVIS ◽

GEORGIANNE TUCKER

Keyword(s):

X Chromosome ◽

Female Mouse ◽

X Chromosome Inactivation ◽

Mouse Embryos ◽

Chromosome Inactivation ◽

X Chromosomes

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Differentiation of X chromosomes in early female mouse embryos

Experimental Cell Research ◽

10.1016/0014-4827(74)90657-0 ◽

1974 ◽

Vol 86 (1) ◽

pp. 127-135 ◽

Cited By ~ 81

Author(s):

N. Takagi

Keyword(s):

Female Mouse ◽

Mouse Embryos ◽

X Chromosomes

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Two maternally derived X chromosomes contribute to parthenogenetic inviability

Development ◽

10.1242/dev.104.1.129 ◽

1988 ◽

Vol 104 (1) ◽

pp. 129-136

Author(s):

J.R. Mann ◽

R.H. Lovell-Badge

Keyword(s):

X Chromosome ◽

Dosage Compensation ◽

Female Mouse ◽

Normal Female ◽

X Chromosomes ◽

Developmental Abnormalities ◽

Series Of Experiments ◽

Preferential Inactivation ◽

Extraembryonic Tissues

In certain extraembryonic tissues of normal female mouse conceptuses, X-chromosome-dosage compensation is achieved by preferential inactivation of the paternally derived X. Diploid parthenogenones have two maternally derived X chromosomes, hence this mechanism cannot operate. To examine whether this contributes to the inviability of parthenogenones, XO and XX parthenogenetic eggs were constructed by pronuclear transplantation and their development assessed after transfer to pseudopregnant recipients. In one series of experiments, the frequency of postimplantation development of XO parthenogenones was much higher than that of their XX counterparts. This result is consistent with the possibility that two maternally derived X chromosomes can contribute to parthenogenetic inviability at or very soon after implantation. However, both XO and XX parthenogenones showed similar developmental abnormalities at the postimplantation stage, demonstrating that parthenogenetic inviability is ultimately determined by the possession of two sets of maternally derived autosomes.

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XO mice

Genetics Research ◽

10.1017/s0016672300003335 ◽

1962 ◽

Vol 3 (3) ◽

pp. 487-490 ◽

Cited By ~ 71

Author(s):

Bruce M. Cattanach

Keyword(s):

Germ Cells ◽

Female Mouse ◽

Early Stage ◽

The Body ◽

The Other ◽

Normal Female ◽

Present Communication ◽

Mouse Development ◽

X Chromosomes ◽

Linked Gene

The inactive-X hypothesis (Lyon, 1961) states that in the normal female mouse only one of the two X chromosomes is genetically active in each cell of the body other than the germ-cells, and that the choice of which X is to be inactivated occurs at an early stage of embryogenesis, and is at random in each cell. The descendants of these cells then abide by the decision so that females are mosaics for two lines of cells and may show a mosaic phenotype if they are heterozygous for a sex-linked gene. One requisite for the validity of this hypothesis is that only one X is necessary for the development of a normal female mouse, and evidence substantiating this supposition is the apparent normality of XO mice (Welshons & Russell, 1959; Cattanach, 1961a, b). On the other hand it has been suggested that XO mice are not fully viable (Russell, Russell & Gower, 1959), but no data on the comparative viability and growth of XO female mice have yet been reported. In the present communication data of this nature, collected in the process of setting up an XO stock, are presented and support the hypothesis that only one X chromosome is necessary for normal female mouse development.

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Neurotransmitter systems of female mouse brain during growth of malignant melanoma modeled on the background of chronic pain

Nauchno-prakticheskii zhurnal «Patogenez» ◽

10.25557/gm.2018.4.9749 ◽

2018 ◽

pp. 49-55

Author(s):

О.И. Кит ◽

И.М. Котиева ◽

Е.М. Франциянц ◽

И.В. Каплиева ◽

Л.К. Трепитаки ◽

...

Keyword(s):

Chronic Pain ◽

Cerebral Cortex ◽

Malignant Melanoma ◽

Sciatic Nerve ◽

Female Mouse ◽

Combined Effects ◽

Malignant Growth ◽

Course Of Disease ◽

The Brain ◽

Melanoma Growth

Известно, что биогенные амины (БА) участвуют в злокачественном росте, их уровень изменяется в ЦНС при болевом воздействии, однако исследований о сочетанном влиянии хронической боли (ХБ) и онкопатологии на динамику БА в головном мозге не проводилось. Цель: изучить особенности баланса БА в коре головного мозга в динамике роста меланомы, воспроизведенной на фоне ХБ. Материалы и методы. Работа выполнена на 64 мышах-самках, весом 21-22 г. Животным основной группы меланому В16/F10 перевивали под кожу спины через 2 недели после перевязки седалищных нервов. Группой сравнения служили мыши с меланомой без боли. Уровни БА: адреналина, норадреналина, дофамина (ДА), серотонина (5-НТ), гистамина, а также 5-ОИУК определяли методом иммуноферментного анализа. Результаты. У мышей с ХБ уменьшается содержание большинства БА, однако уровень ДА не изменяется. Метаболизм 5-НТ происходит с участием МАО. Развитие меланомы сопровождается увеличением содержания ДА и 5-НТ, тогда как МАО - ингибируется. Направленность сдвигов БА при развитии меланомы на фоне ХБ оказалась практически такой же, как и без неё. В то же время ХБ ограничивает накопление 5-НТ в коре мозга при меланоме, что сопровождается более агрессивным её течением. Выводы. ХБ ограничивает включение стресс-лимитирующих механизмов в головном мозге при развитии меланомы у мышей, что приводит к более агрессивному течению злокачественного процесса. Biogenic amines (BA) are known to be involved in malignant growth, and their CNS levels change in pain; however, there are no studies of combined effects of chronic pain (CP) and cancer on BA dynamics in the brain. Aim: To study features of BA balance in the cerebral cortex during melanoma growth associated with CP. Material and methods. The study included 64 female mice weighing 21-22 g. In the main groups, B16/F10 melanoma was transplanted under the skin of the back two weeks following sciatic nerve ligation. Mice with melanoma without pain were used as the control. Concentrations of BA: adrenaline, noradrenaline, dopamine (DA), serotonin (5-HT), histamine and 5-HIAA were measured with ELISA. Results. Concentrations of BAs decreased in mice with CP although DA levels did not change. 5-HT metabolism involved MAO. The development of melanoma was accompanied by increases in DA and 5-HT whereas MAO was inhibited. The direction of BA changes during the development of melanoma was the same with and without CP. At the same time, CP with melanoma limited accumulation of 5-HT in the cerebral cortex, which resulted in even more aggressive course of cancer. Conclusion. CP restricted the activation of cerebral stress-limiting mechanisms during the development of melanoma in mice, which resulted in a more aggressive course of disease.

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