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 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 Single Cell Analysis Reveals Partial Reactivation of X-chromosome Instead of Chromosome-wide Dampening in Naïve Human Pluripotent Stem Cells

2019 ◽  
Author(s):  
S Mandal ◽  
D Chandel ◽  
H Kaur ◽  
S Majumdar ◽  
M Arava ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Single Cell ◽  
X Chromosome ◽  
Pluripotent Stem Cells ◽  
Single Cell Analysis ◽  
Human Pluripotent Stem Cells ◽  
Preimplantation Embryos ◽  
X Chromosomes ◽  
Linked Gene

AbstractRecently, a unique form of X-chromosome dosage compensation has been demonstrated in human preimplantation embryos, which happens through the dampening of X-linked gene expression from both X-chromosomes. Subsequently, X-chromosome dampening has also been demonstrated in female human pluripotent stem cells (hPSCs) during the transition from primed to naïve state. However, the existence of dampened X-chromosomes remains controversial in both embryos and hPSCs. Specifically, in preimplantation embryos it has been shown that there is inactivation of X-chromosome instead of dampening. Here, we have performed allelic analysis of X-linked genes at the single cell level in hPSCs and found that there is partial reactivation of the inactive X-chromosome instead of chromosome-wide dampening upon conversion from primed to naïve state. In addition, our analysis suggests that the reduced X-linked gene expression in naïve hPSCs might be the consequence of erasure of active X-chromosome upregulation.

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.

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.

Expression of SRG3, a chromatin-remodelling factor, in the mouse oocyte and early preimplantation embryos

Zygote ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 129-138 ◽  
Author(s):  
F. Sun ◽  
F. Tang ◽  
A Y. Yan ◽  
H. Y. Fang ◽  
H. Z. Sheng
Keyword(s):  
Essential Role ◽  
Structure And Function ◽  
Chromatin Remodelling ◽  
Preimplantation Embryos ◽  
Protein Synthesis Inhibitor ◽  
Mouse Development ◽  
Synthesis Inhibitor ◽  
Female Pronucleus ◽  
Early Mouse ◽  
And Function

SummarySRG3 (Smarcc1) is a core subunit of the SWI/SNF complex. In the absence of SRG3, embryonic development ceases during peri-implantation stages, indicating that SRG3, as well as the chromatin-remodelling process, plays an essential role in early mouse development. To gain a better understanding of chromatin remodelling during the early stages of development, we examined SRG3 expression during oogenesis and preimplantation stages using immunofluorescence and western blot assays. SRG3 was detected in nuclei of oocytes during growth and maturation. Following fertilization, SRG3 was detected in pronuclei shortly after their formation. Nuclear concentrations of SRG3 increased in a time-dependent fashion and were found to be greater in the male pronucleus than in the female pronucleus. The increase in nuclear SRG3 was partially inhibited by a protein synthesis inhibitor, but not by a transcriptional inhibitor. Expression of SRG3 is accompanied by expression of Brg1 and Ini1, two other core subunits of the SWI/SNF complex. The expression of these three remodelling factors parallels that of SP1 and TBP, both spatially and temporally, in the mouse embryo, suggesting a role for remodelling factors in chromatin structure and function during early development.

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.

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