scholarly journals The lncRNA Locus Handsdown Regulates Cardiac Gene Programs and Is Essential for Early Mouse Development

2019 ◽  
Vol 50 (5) ◽  
pp. 644-657.e8 ◽  
Author(s):  
Nicole Ritter ◽  
Tamer Ali ◽  
Nina Kopitchinski ◽  
Peggy Schuster ◽  
Arica Beisaw ◽  
...  
Keyword(s):  
Mouse Development ◽  
Lncrna Locus ◽  
Cardiac Gene ◽  
Early Mouse

scholarly journals 03-P119 Decipher β-catenin functions in early mouse development

2009 ◽  
Vol 126 ◽  
pp. S101-S102
Author(s):  
Stefan Rudloff ◽  
Rolf Kemler
Keyword(s):  
Mouse Development ◽  
Early Mouse

Targets and dynamics of promoter DNA methylation during early mouse development

2010 ◽  
Vol 42 (12) ◽  
pp. 1093-1100 ◽  
Author(s):  
Julie Borgel ◽  
Sylvain Guibert ◽  
Yufeng Li ◽  
Hatsune Chiba ◽  
Dirk Schübeler ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mouse Development ◽  
Promoter Dna Methylation ◽  
Promoter Dna ◽  
Early Mouse

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

The Foxh1-dependent autoregulatory enhancer controls the level of Nodal signals in the mouse embryo

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3455-3468 ◽  
Author(s):  
Dominic P. Norris ◽  
Jane Brennan ◽  
Elizabeth K. Bikoff ◽  
Elizabeth J. Robertson
Keyword(s):  
Mouse Embryo ◽  
Late Onset ◽  
Axis Formation ◽  
Visceral Endoderm ◽  
Mouse Development ◽  
Developmental Abnormalities ◽  
Intronic Enhancer ◽  
Vertebrate Embryo ◽  
Early Mouse ◽  
Pitx2 Expression

The TGFβ-related growth factor Nodal governs anteroposterior (AP) and left-right (LR) axis formation in the vertebrate embryo. A conserved intronic enhancer (ASE), containing binding sites for the fork head transcription factor Foxh1, modulates dynamic patterns of Nodal expression during early mouse development. This enhancer is responsible for early activation of Nodal expression in the epiblast and visceral endoderm, and at later stages governs asymmetric expression during LR axis formation. We demonstrate ASE activity is strictly Foxh1 dependent. Loss of this autoregulatory enhancer eliminates transcription in the visceral endoderm and decreases Nodal expression in the epiblast, but causes surprisingly discrete developmental abnormalities. Thus lowering the level of Nodal signaling in the epiblast disrupts both orientation of the AP axis and specification of the definitive endoderm. Targeted removal of the ASE also dramatically reduces left-sided Nodal expression, but the early events controlling LR axis specification are correctly initiated. However loss of the ASE disrupts Lefty2 (Leftb) expression and causes delayed Pitx2 expression leading to late onset, relatively minor LR patterning defects. The feedback loop is thus essential for maintenance of Nodal signals that selectively regulate target gene expression in a temporally and spatially controlled fashion in the mouse embryo.

Cell division and cell allocation in early mouse development

Development ◽  
1978 ◽  
Vol 48 (1) ◽  
pp. 37-51
Author(s):  
S. J. Kelly ◽  
J. G. Mulnard ◽  
C. F. Graham
Keyword(s):  
Cell Division ◽  
Tritiated Thymidine ◽  
Mouse Embryos ◽  
Mouse Development ◽  
Stages Of Development ◽  
Cell Stage ◽  
Cell Cycles ◽  
Short Cell ◽  
Early Mouse

Cell division was observed in intact and dissociated mouse embryos between the 2-cell stage and the blastocyst in embryos developing in culture. Division to the 4-cell stage was usually asynchronous. The first cell to divide to the 4-cell stage produced descendants which tended to divide ahead of those cells produced by its slow partner at all subsequent stages of development up to the blastocyte stage. The descendants of the first cell to divide to the 4-cell stage did not subsequently have short cell cycles. The first cell or last cell to divide from the 4-cell stage was labelled with tritiated thymidine. The embryo was reassembled, and it was found that the first pair of cells to reach the 8-cell stage contributed disproportionately more descendants to the ICM when compared with the last cell to divide to the 8-cell stage.

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.

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