scholarly journals Parental imprinting on the mouse X chromosome: effects on the early development of X0, XXY and XXX embryos

1993 ◽  
Vol 62 (2) ◽  
pp. 139-148 ◽  
Author(s):  
Takashi Tada ◽  
Nobuo Takagi ◽  
Ilse-Dore Adler
Keyword(s):  
X Chromosome ◽  
Cytogenetic Study ◽  
Abnormal Development ◽  
Mouse Strains ◽  
Mouse Embryogenesis ◽  
Linked Gene ◽  
Parental Imprinting ◽  
Early Mouse ◽  
The One ◽  
Chromosome Imprinting

SummaryTo examine the effects of X-chromosome imprinting during early mouse embryogenesis, we attempted to produce XM0, Xp0, XMXMY, XMXPY and XMXMXP (where XM and Xp stand for the maternally and the paternally derived X chromosome, respectively) making use of mouse strains bearing the translocation Rb(X.2)2Ad and the inversion In(X)1H. Unlike XMXPY embryos, XMXMY and XMXMXP conceptuses suffered from severe growth retardation or abnormal development characterized by deficient extra-embryonic structures at 6.5–7.5 days post coitum (dpc). A cytogenetic study suggested that two XM chromosomes remaining active in certain non-epiblast cells were responsible for the serious developmental abnormality found in these embryos disomic for XM. Although matings involving females heterozygous for Rb(X.2)2Ad hinted at the paucity of XP0 embryos relative to those having the complementary karyotype of XMXMXP, further study of embryos from matings between females heterozygous for In(X)1H and Rb2Ad males did not substantiate this observation. Thus, the extensive peri-implantation loss of XP0 embryos shown by Hunt (1991) may be confined to XO mothers. Taken together, this study failed to reveal a parentally imprinted X-linked gene essential for early mouse embryogenesis other than the one most probably corresponding to the X-chromosome inactivation centre.

scholarly journals Regulation of X-linked gene expression during early mouse development by Rlim

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Feng Wang ◽  
JongDae Shin ◽  
Jeremy M Shea ◽  
Jun Yu ◽  
Ana Bošković ◽  
...  
Keyword(s):  
Gene Expression ◽  
X Chromosome ◽  
Gene Dosage ◽  
Mouse Genetics ◽  
Preimplantation Embryos ◽  
Mouse Development ◽  
Linked Gene ◽  
Temporal Regulation ◽  
Non Coding Rna ◽  
Early Mouse

Mammalian X-linked gene expression is highly regulated as female cells contain two and male one X chromosome (X). To adjust the X gene dosage between genders, female mouse preimplantation embryos undergo an imprinted form of X chromosome inactivation (iXCI) that requires both Rlim (also known as Rnf12) and the long non-coding RNA Xist. Moreover, it is thought that gene expression from the single active X is upregulated to correct for bi-allelic autosomal (A) gene expression. We have combined mouse genetics with RNA-seq on single mouse embryos to investigate functions of Rlim on the temporal regulation of iXCI and Xist. Our results reveal crucial roles of Rlim for the maintenance of high Xist RNA levels, Xist clouds and X-silencing in female embryos at blastocyst stages, while initial Xist expression appears Rlim-independent. We find further that X/A upregulation is initiated in early male and female preimplantation embryos.

scholarly journals Live imaging of X chromosome reactivation dynamics in early mouse development can discriminate naïve from primed pluripotent stem cells

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  
Keyword(s):  
Stem Cells ◽  
X Chromosome ◽  
Pluripotent Stem Cells ◽  
Live Imaging ◽  
Mouse Development ◽  
Early Mouse

Detrimental effects of two active X chromosomes on early mouse development

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 189-201 ◽  
Author(s):  
N. Takagi ◽  
K. Abe
Keyword(s):  
X Chromosome ◽  
Distal Segment ◽  
Translocation Chromosome ◽  
Mouse Development ◽  
X Chromosomes ◽  
Developmental Abnormalities ◽  
Inactivation Center ◽  
Normal Males ◽  
Early Mouse ◽  
Embryonic Ectoderm

Matings between female mice carrying Searle's translocation, T(X;16)16H, and normal males give rise to chromosomally unbalanced zygotes with two complete sets of autosomes, one normal X chromosome and one X16 translocation chromosome (XnX16 embryos). Since X chromosome inactivation does not occur in these embryos, probably due to the lack of the inactivation center on X16, XnX16 embryos are functionally disomic for the proximal 63% of the X chromosome and trisomic for the distal segment of chromosome 16. Developmental abnormalities found in XnX16 embryos include: (1) growth retardation detected as early as stage 9, (2) continual loss of embryonic ectoderm cells either by death or by expulsion into the proamniotic cavity, (3) underdevelopment of the ectoplacental cone throughout the course of development, (4) very limited, if any, mesoderm formation, (5) failure in early organogenesis including the embryo, amnion, chorion and yolk sac. Death occurred at 10 days p.c. Since the combination of XO and trisomy 16 does not severely affect early mouse development, it is likely that regulatory mechanisms essential for early embryogenesis do not function correctly in XnX16 embryos due to activity of the extra X chromosome segment of X16.

The tabby syndrome in the mouse

1971 ◽  
Vol 179 (1055) ◽  
pp. 139-156 ◽  
Keyword(s):  
Critical Point ◽  
X Chromosome ◽  
Neural Tube ◽  
X Chromosome Inactivation ◽  
Cellular Level ◽  
Normal Allele ◽  
Linked Gene ◽  
Intercellular Interactions ◽  
Threshold Mechanism ◽  
Otic Vesicles

The tabby syndrome in the mouse (which is common to the sex-linked gene for tabby and autosomal genes for crinkled and downless) affects the coat, the sinus hairs, the teeth, many glands and some surface features like tail rings, plicae digitales and the papilla vallata of the tongue. All these structures develop by the downgrowth of solid epithelial buds into the underlying mesenchyme. Organs which arise by invagination (like the neural tube or the otic vesicles and certain glands) are not affected by the tabby syndrome. The rudiments of glands and sinus hairs are reduced in size, and if reduction goes beyond a critical point, stunted organs are formed or, more commonly, the rudiments regress altogether. The same is true for the teeth and apparently for the whole syndrome. Measurements show the same situation in Ta ♂♂(and Ta/Ta ♀♀) and in heterozygous Ta / + ♀♀. As in Ta ♂♂ and Ta/Ta ♀♀ there cannot be any doubt that a threshold mechanism is involved, there is no reason to assume that, in Ta / + ♀♀, the identical defects are derived clonally from ancestral cells in which the Xchromosome carrying the normal allele has been inactivated. Whereas the Ta / + phenotype does not give any evidence that the Ta locus is involved in X-chromosome inactivation, the possibility cannot be ruled out that, if inactivation should actually take place on the cellular level, the macroscopic phenotype could be the result of intercellular interactions along with the effects of threshold mechanisms.

scholarly journals Author response: Regulation of X-linked gene expression during early mouse development by Rlim

2016 ◽  
Author(s):  
Feng Wang ◽  
JongDae Shin ◽  
Jeremy M Shea ◽  
Jun Yu ◽  
Ana Bošković ◽  
...  
Keyword(s):  
Gene Expression ◽  
Author Response ◽  
Mouse Development ◽  
Linked Gene ◽  
Early Mouse

scholarly journals Dynamic GATA6 expression in primitive endoderm formation and maturation in early mouse embryogenesis

2008 ◽  
Vol 237 (10) ◽  
pp. 2820-2829 ◽  
Author(s):  
Kathy Q. Cai ◽  
Callinice D. Capo-Chichi ◽  
Malgorzata E. Rula ◽  
Dong-Hua Yang ◽  
Xiang-Xi Xu
Keyword(s):  
Primitive Endoderm ◽  
Mouse Embryogenesis ◽  
Early Mouse

Lack of inactivation of a mouse X-linked gene physically separated from the inactivation centre

Development ◽  
1986 ◽  
Vol 97 (1) ◽  
pp. 75-85
Author(s):  
Mary F. Lyon ◽  
J. Zenthon ◽  
E. P. Evans ◽  
M. D. Burtenshaw ◽  
Kathryn A. Wareham ◽  
...  
Keyword(s):  
X Chromosome ◽  
Normal Animal ◽  
Histochemical Staining ◽  
X Inactivation ◽  
Chromosome Break ◽  
Linked Gene ◽  
Short Product ◽  
Chromosome Segments ◽  
Harmful Effects

Previous evidence had shown that, when a mammalian X-chromosome is broken by a translocation, only one of the two X-chromosome segments shows cytological signs of X-inactivation in the form of late replication or Kanda staining. In the two mouse X-autosome translocations T(X;4)37H and T(X;11)38H the X-chromosome break is in the A1–A2 bands; in both, the shorter translocation product fails to exhibit Kanda staining. By in situ hybridization, the locus of ornithine carbamoyltransferase (OCT) was shown to be proximal to the breakpoint (i.e. on the short product) in T37H and distal to the breakpoint in T38H. Histochemical staining for OCT showed that in T38H the locus of OCT undergoes random inactivation, as in a chromosomally normal animal, whereas in T37H the OCT locus remains active in all cells. The interpretation is that, when a segment of X-chromosome is physically separated from the X-inactivation centre, it fails to undergo inactivation. This point is important for the understanding of the mechanism of X-inactivation, since it implies that inactivation is a positive process, brought about by some event that travels along the chromosome. It is also relevant to the interpretation of the harmful effects of X-autosome translocations and the abnormalities seen in individuals carrying such translocations.

Drosophila Male-Specific Lethal 2 Protein Controls Sex-Specific Expression of the roX Genes

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1825-1832 ◽  
Author(s):  
Barbara P Rattner ◽  
Victoria H Meller
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
X Chromosome ◽  
Specific Expression ◽  
Linked Gene ◽  
Male And Female ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific ◽  
Rox Rna

Abstract The MSL complex of Drosophila upregulates transcription of the male X chromosome, equalizing male and female X-linked gene expression. Five male-specific lethal proteins and at least one of the two noncoding roX RNAs are essential for this process. The roX RNAs are required for the localization of MSL complexes to the X chromosome. Although the mechanisms directing targeting remain speculative, the ratio of MSL protein to roX RNA influences localization of the complex. We examine the transcriptional regulation of the roX genes and show that MSL2 controls male-specific roX expression in the absence of any other MSL protein. We propose that this mechanism maintains a stable MSL/roX ratio that is favorable for localization of the complex to the X chromosome.

Sign in / Sign up

Export Citation Format

Share Document