Preferential inactivation of the paternally derived X chromosome in the extraembryonic membranes of the mouse

Nature ◽  
1975 ◽  
Vol 256 (5519) ◽  
pp. 640-642 ◽  
Author(s):  
NOBUO TAKAGI ◽  
MOTOMICHI SASAKI
Keyword(s):  
X Chromosome ◽  
Extraembryonic Membranes ◽  
Preferential Inactivation

X chromosome retains the memory of its parental origin in murine embryonic stem cells

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 813-821 ◽  
Author(s):  
T. Tada ◽  
M. Tada ◽  
N. Takagi
Keyword(s):  
X Chromosome ◽  
Polar Region ◽  
Biochemical Study ◽  
Es Cells ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Parental Origin ◽  
Visceral Endoderm ◽  
Es Cell ◽  
Preferential Inactivation

A cytogenetic and biochemical study of balloon-like cystic embryoid bodies, formed by newly established embryonic stem (ES) cell lines having a cytogenetically or genetically marked X chromosome, revealed that the paternally derived X chromosome was inactivated in the majority of cells in the yolk sac-like mural region consisting of the visceral endoderm and mesoderm. The nonrandomness was less evident in the more solid polar region containing the ectodermal vesicle, mesoderm and visceral endoderm. Since the same was true in embryoid bodies derived from ES cells at the 30th subculture generation, it was concluded that the imprinting responsible for the preferential inactivation of the paternal X chromosome that was limited to non-epiblast cells of the female mouse embryos, was stably maintained in undifferentiated ES cells. Differentiating epiblast cells should be able to erase or avoid responding to the imprint.

scholarly journals Expression and Linkage of Genes for X-linked Hemophilias A and B in the Dog

Blood ◽  
1973 ◽  
Vol 41 (4) ◽  
pp. 577-585 ◽  
Author(s):  
K. M. Brinkhous ◽  
P. D. Davis ◽  
John B. Graham ◽  
W. Jean Dodds
Keyword(s):  
X Chromosome ◽  
Hemophilia A ◽  
Factor Ix ◽  
Neonatal Lethality ◽  
Plasma Factor ◽  
Normal Males ◽  
Linkage Of Genes ◽  
Linkage Distance ◽  
Antihemophilic Factor ◽  
Preferential Inactivation

Abstract The linkage distance on the X chromosome between the genes for hemophilia A (classic hemophilia) and B (PTC deficiency, Christmas disease) was estimated directly by breeding two strains of dogs, each segregating for a different type of hemophilia. Gene expression was determined by bioassays of plasma factor VIII (antihemophilic factor) and factor IX (PTC, Christmas factor). Double heterozygotes in repulsion for both hemophilia A and B could be readily identified by intermediate plasma levels of both procoagulants. There was no evidence of a tendency toward preferential inactivation of the paternally derived X chromosome, and the procoagulant levels showed that random inactivation had occurred at both loci. When double heterozygotes were bred against normal males or males with hemophilia A and B, the progeny that resulted indicated that the genes recombined freely. Thus, the genes are at least 50 map units apart. The phenotypes of five new hemophilic genotypes are described as a result of the various crossbreedings, including males with double hemophilia AB. When both hemophilia genes are in the coupling phase, there is evidence of increased intrauterine or neonatal lethality in males. The data from this study, along with that on gene linkage of human hemophilia A and B, provide support for the thesis of homology of the X chromosome during speciation.

Preferential paternal X inactivation in extraembryonic tissues of early mouse embryos

Development ◽  
1982 ◽  
Vol 67 (1) ◽  
pp. 127-135
Author(s):  
Mary I. Harper ◽  
Mandy Fosten ◽  
Marilyn Monk
Keyword(s):  
X Chromosome ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Phosphoglycerate Kinase ◽  
X Inactivation ◽  
Preferential Expression ◽  
Trophoblastic Cells ◽  
Extraembryonic Membranes ◽  
Early Mouse

The preferential expression of the maternal X chromosome seen in certain extraembryonic membranes of the mouse was studied by investigating the tissues from which these membranes are derived during early development. The electrophoretic variant of the X-coded enzyme PGK-1 (phosphoglycerate kinase) was used to distinguish the expression of the maternal from the paternal X chromosome in heterozygous females. Both the extraembryonic ectoderm and primary endoderm of 6½-day female egg cylinders gave almost exclusive expression of the maternal form of the enzyme whereas the epiblast gave near equal expression of the two parental alleles. No paternal PGK-1 band could be detected in samples of pooled 3½-day blastocysts, but after 3 or 4 days of culture in vitro a faint paternal band was seen in the resultant outgrowths. The activity of the maternal band in these latter samples had increased greatly from that of the blastocysts, consistent with preferential expression of the maternal Pgk-1 allele in the trophoblastic cells of the outgrowths, while both alleles are expressed in inner-cell-mass cells. The results strongly support the idea that non-random X-chromosome expression is due to preferential paternal X inactivation in trophectoderm (from which extraembryonic ectoderm is derived) and in primary endoderm, and not to cell selection.

Genetic activity at the albino locus in Cattanach's insertion in the mouse

Development ◽  
1986 ◽  
Vol 96 (1) ◽  
pp. 295-302
Author(s):  
M. S. Deol ◽  
Gillian M. Truslove ◽  
Anne McLaren
Keyword(s):  
X Chromosome ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
The Other ◽  
Normal Allele ◽  
Cell Type ◽  
Direct Examination ◽  
Autosome Translocation ◽  
Genetic Activity ◽  
Preferential Inactivation

Cattanach's insertion (Is(In7;X)1Ct or XCt) includes the normal allele at the albino locus (c+), which is subject to inactivation of the X chromosome carrying it, so that XCtX; c c mice have albino and pigmented patches. The X-autosome translocation T(X;16)16H or XT16H leads to preferential inactivation of the other X chromosome in female cells, so that XCtXT16H; c c mice are almost entirely white. However, they grow darker with age, as if reversal of inactivation of the c+ allele were taking place in increasing numbers of melanocytes. To test whether this is dependent only on age or whether it is related to the number of times the animal has moulted, hair was repeatedly plucked from selected areas at the early telogen stage when the follicles are also removed, assuming that the melanocytes or melanoblasts in that region of the skin would be forced to undergo further divisions to colonize the new follicles. The plucked areas grew darker at the same rate as the rest of the coat, suggesting that the progressive reversal of inactivation is dependent only on age. As direct examination of melanocytes in the follicles is difficult, they were examined in the choroid and the retinal pigment epithelium (RPE) of the eye. The frequency of the pigmented cells was lower in the choroid than in the RPE. Since the melanocytes in these structures are different in origin as well as in physical characteristics, it appears that cell type influences either reversal of inactivation, or the frequency with which the influence of the X chromosome extends to the albino locus.

scholarly journals The development of XO gynogenetic mouse embryos

Development ◽  
1987 ◽  
Vol 99 (3) ◽  
pp. 411-416
Author(s):  
J.R. Mann ◽  
R.H. Lovell-Badge
Keyword(s):  
X Chromosome ◽  
Mouse Embryos ◽  
Nuclear Transplantation ◽  
Normal Female ◽  
Cell Stage ◽  
X Chromosomes ◽  
Extraembryonic Membranes ◽  
Chromosome Imprinting

Diploid gynogenetic embryos, which have two sets of maternal and no paternal chromosomes, die at or soon after implantation. Since normal female embryos preferentially inactivate the paternally derived X chromosome in certain extraembryonic membranes, the inviability of diploid gynogenetic embryos might be due to difficulties in achieving an equivalent inactivation of one of their two maternally derived X chromosomes. In order to investigate this possibility, we constructed XO gynogenetic embryos by nuclear transplantation at the 1-cell stage. These XO gynogenones showed the same mortality around the time of implantation as did their XX gynogenetic counterparts. This shows that the lack of a paternally derived autosome set is sufficient to cause gynogenetic inviability at this stage. Autosomal imprinting and its possible relation to X-chromosome imprinting is discussed.

Moderate haemophilia B in a female carrier caused by preferential inactivation of the paternal X chromosome

2009 ◽  
Vol 47 (4) ◽  
pp. 257-261 ◽  
Author(s):  
Stefan Kling ◽  
Alison J. Coffey ◽  
Rolf Ljung ◽  
Elsy Sjorin ◽  
Inga Marie Nilsson ◽  
...  
Keyword(s):  
X Chromosome ◽  
Female Carrier ◽  
Haemophilia B ◽  
Preferential Inactivation

Paternal X chromosome expression in extraembryonic membranes of XO mice

1979 ◽  
Vol 210 (3) ◽  
pp. 553-560 ◽  
Author(s):  
William I. Frels ◽  
Verne M. Chapman
Keyword(s):  
X Chromosome ◽  
Extraembryonic Membranes

Evidence of a preferential inactivation of the paternally derived X chromosome in a 46,XX true hermaphrodite

1985 ◽  
Vol 69 (1) ◽  
pp. 91-93 ◽  
Author(s):  
C. Boucekkine ◽  
D. Nafa ◽  
M. Casanova-Bettane ◽  
F. Latron ◽  
M. Fellous ◽  
...  
Keyword(s):  
X Chromosome ◽  
True Hermaphrodite ◽  
Preferential Inactivation

An extra maternally derived X chromosome is deleterious to early mouse development

Development ◽  
1990 ◽  
Vol 110 (3) ◽  
pp. 969-975 ◽  
Author(s):  
C. Shao ◽  
N. Takagi
Keyword(s):  
X Chromosome ◽  
Early Death ◽  
X Inactivation ◽  
Mouse Development ◽  
Extra Copy ◽  
X Chromosomes ◽  
Extraembryonic Membranes ◽  
Early Mouse ◽  
Ectoplacental Cone ◽  
Embryonic Death

An extra copy of the X chromosome, unlike autosomes, exerts only minor effects on development in mammals including man and mice, because all X chromosomes except one are genetically inactivated. Contrary to this contention, we found that an additional maternally derived X (XM) chromosome, but probably not a paternally derived one (XP), consistently contributes to early death of 41,XXY and 41,XXX embryos in mice. Because of imprinted resistance to inactivation, two doses of XM remain active in the trophectoderm, and seem to be responsible for the failure in the development of the ectoplacental cone and extraembryonic ectoderm, and hence, from early embryonic death. Discordant observations in man indicating viability of XMXMXP and XMXMY individuals suggest that imprinting on the human X chromosome is either weak, unstable or erased before the initiation of X-inactivation in progenitors of extraembryonic membranes.

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