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.

RNA synthesis at the two-cell stage of mouse development

Development ◽  
1972 ◽  
Vol 27 (1) ◽  
pp. 167-176
Author(s):  
John Knowland ◽  
Chris Graham
Keyword(s):  
Nucleic Acids ◽  
Rna Synthesis ◽  
Mouse Embryos ◽  
Rrna Synthesis ◽  
Mouse Development ◽  
Cell Stage ◽  
Electrophoretic Mobilities ◽  
Quantitative Extraction ◽  
Early Mouse ◽  
Embryonic Fibroblast

This paper describes a method for quantitative extraction of nucleic acids from cultured pre-implantation mouse embryos in a form suitable for electrophoresis, and its application to the analysis of RNA synthesized during early mouse development. The nucleic acids synthesized by early mouse embryos have been identified by the use of RNase, DNase and mild alkaline hydrolysis. No obvious differences in the kinds of RNA synthesized in the blastocyst, trophoblast or embryonic fibroblast were found. At the two-cell stage of mouse development, which is the earliest that can be successfully labelled with radioactive precursors of RNA, all major RNA classes with similar electrophoretic mobilities to the RNA species of adult cells are synthesized, and it is likely that 28 s and 18 s RNA are synthesized at this stage. It is suggested that the onset of rRNA synthesis may not be associated with a particular stage of embryonic development.

Localisation of tight junction protein cingulin is temporally and spatially regulated during early mouse development

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1135-1144 ◽  
Author(s):  
T.P. Fleming ◽  
M. Hay ◽  
Q. Javed ◽  
S. Citi
Keyword(s):  
Tight Junction ◽  
Cell Types ◽  
Early Embryo ◽  
Mouse Development ◽  
Cell Stage ◽  
Tight Junction Formation ◽  
Junction Protein ◽  
Junction Site ◽  
Mouse Early Embryo ◽  
Early Mouse

The molecular maturation of the tight junction in the mouse early embryo has been investigated by monitoring the distribution of cingulin, a 140 × 10(3) M(r) peripheral (cytoplasmic) membrane constituent of the junction, at different stages of development and in different experimental situations. Although tight junction formation does not begin until compaction at the 8-cell stage, cingulin is detectable in oocytes and all stages of cleavage, a factor consistent with our biochemical analysis of cingulin expression (Javed et al., 1992, Development 117, 1145–1151). Using synchronised egg and embryo stages and isolated cell clusters, we have identified three sites where cingulin is localised, the cytocortex, punctate cytoplasmic foci and tight junctions themselves. Cytocortical cingulin is present at the cumulus-oocyte contact site (both cell types), in unfertilised and fertilised eggs and in cleavage stages up to 16-cell morulae, particularly at microvillous domains on the embryo outer surface (eg. apical poles at compaction). Embryo manipulation experiments indicate that cortical cingulin is labile and dependent upon cell interactions and therefore is not merely an inheritance from the egg. Cingulin cytoplasmic foci are evident only in outer cells (prospective trophectoderm) from the 32-cell stage, just prior to cavitation, and decline from approx. 8 hours after cavitation has initiated. The appearance of these foci is insensitive to cycloheximide treatment and they colocalise with apically derived endocytic vesicles visualised by FITC-dextran, indicating that the foci represent the degradation of cytocortical cingulin by endocytic turnover. Cingulin is detectable at the tight junction site between blastomeres usually from the 16-cell stage, although earlier assembly occurs in a minority (up to 20%) of specimens. Cingulin assembly at the tight junction is sensitive to cycloheximide and is identifiable approx. 10 hours after cell adhesion is initiated and ZO-1 protein assembles. Collectively, our results indicate that (i) cingulin from nonjunctional sites does not contribute to tight junction assembly and (ii) the molecular maturation of the junction appears to occur progressively over at least two cell cycles.

scholarly journals AGS3-dependent trans-Golgi network membrane trafficking is essential for compaction in mouse embryos

2020 ◽  
Vol 133 (23) ◽  
pp. jcs243238
Author(s):  
Zheng-Wen Nie ◽  
Ying-Jie Niu ◽  
Wenjun Zhou ◽  
Dong-Jie Zhou ◽  
Ju-Yeon Kim ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Membrane Trafficking ◽  
Fluorescent Protein ◽  
Mouse Embryos ◽  
Cell Contact ◽  
Protein Signaling ◽  
Cell Stage ◽  
Trans Golgi Network ◽  
Early Mouse ◽  
Golgi Network

ABSTRACTActivator of G-protein signaling 3 (AGS3, also known as GPSM1) regulates the trans-Golgi network. The AGS3 GoLoco motif binds to Gαi and thereby regulates the transport of proteins to the plasma membrane. Compaction of early embryos is based on the accumulation of E-cadherin (Cdh1) at cell-contacted membranes. However, how AGS3 regulates the transport of Cdh1 to the plasma membrane remains undetermined. To investigate this, AGS3 was knocked out using the Cas9-sgRNA system. Both trans-Golgi network protein 46 (TGN46, also known as TGOLN2) and transmembrane p24-trafficking protein 7 (TMED7) were tracked in early mouse embryos by tagging these proteins with a fluorescent protein label. We observed that the majority of the AGS3-edited embryos were developmentally arrested and were fragmented after the four-cell stage, exhibiting decreased accumulation of Cdh1 at the membrane. The trans-Golgi network and TMED7-positive vesicles were also dispersed and were not polarized near the membrane. Additionally, increased Gαi1 (encoded by GNAI1) expression could rescue AGS3-overexpressed embryos. In conclusion, AGS3 reinforces the dynamics of the trans-Golgi network and the transport of TMED7-positive cargo containing Cdh1 to the cell-contact surface during early mouse embryo development.

Phosphorylation of mitogen-activated protein kinase cascade during early embryo development in the mouse

2000 ◽  
Vol 12 (4) ◽  
pp. 209 ◽  
Author(s):  
Naoki Iwamori ◽  
Kunihiko Naito ◽  
Koji Sugiura ◽  
Hideyuki Kagii ◽  
Masakane Yamashita ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Embryo Development ◽  
Somatic Cells ◽  
Mouse Embryos ◽  
Mapk Cascade ◽  
Mitogen Activated Protein Kinase ◽  
Cell Stage ◽  
Mitogen Activated Protein ◽  
Early Mouse

The mitogen-activated protein kinase (MAPK) cascade is one of the most important signal transduction pathways that regulate the cell cycle in somatic cells. The present study examined the phosphorylation states of components in the MAPK cascade, Raf-1, MEK-1, and extracellular signal regulated kinases (ERKs), which are activated by mitogens, throughout early mouse embryo development and in cultured somatic cells generally. In somatic cells, Raf-1 and MEK-1 were phosphorylated at M-phase and dephosphorylated during interphase. ERKs were not phosphorylated at any stage during the cell cycle. These results were similar to previous findings for the first and second cell cycles of early mouse embryos. In contrast, after the four-cell stage, not only ERKs, but also Raf-1 and MEK-1, were not phosphorylated at any stage during the cell cycle in mouse early embryos. These results suggest that the MAPK cascade in mouse embryos is regulated by the same mechanism as in somatic cells before the two-cell stage, and that regulation is changed to an embryo-specific mechanism after the four-cell stage.

Focal adhesion kinase PTK2 autophosphorylation is not required for the activation of sodium–hydrogen exchange by decreased cell volume in the preimplantation mouse embryo

Zygote ◽  
2019 ◽  
Vol 27 (3) ◽  
pp. 173-179
Author(s):  
Jane C. Fenelon ◽  
Baozeng Xu ◽  
Jay M. Baltz
Keyword(s):  
Focal Adhesion Kinase ◽  
Cell Volume ◽  
Focal Adhesion ◽  
Mouse Embryo ◽  
Hydrogen Exchange ◽  
Cell Types ◽  
Mouse Embryos ◽  
Cell Stage ◽  
Early Embryos ◽  
Early Mouse

SummaryRecovery from decreased cell volume is accomplished by a regulated increase of intracellular osmolarity. The acute response is activation of inorganic ion transport into the cell, the main effector of which is the Na+/H+ exchanger NHE1. NHE1 is rapidly activated by a cell volume decrease in early embryos, but how this occurs is incompletely understood. Elucidating cell volume-regulatory mechanisms in early embryos is important, as it has been shown that their dysregulation results in preimplantation developmental arrest. The kinase JAK2 has a role in volume-mediated NHE1 activation in at least some cells, including 2-cell stage mouse embryos. However, while 2-cell embryos show partial inhibition of NHE1 when JAK2 activity is blocked, NHE1 activation in 1-cell embryos is JAK2-independent, implying a requirement for additional signalling mechanisms. As focal adhesion kinase (FAK aka PTK2) becomes phosphorylated and activated in some cell types in response to decreased cell volume, we sought to determine whether it was involved in NHE1 activation in the early mouse embryo. FAK activity requires initial autophosphorylation of a tyrosine residue, Y397. However, FAK Y397 phosphorylation levels were not increased in either 1- or 2-cell embryos after cell volume was decreased. Furthermore, the selective FAK inhibitor PF-562271 did not affect NHE1 activation at concentrations that essentially eliminated Y397 phosphorylation. Thus, autophosphorylation of FAK Y397 does not appear to be required for NHE1 activation induced by a decrease in cell volume in early mouse embryos.

scholarly journals G9a regulates temporal preimplantation developmental program and lineage segregation in blastocyst

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jan J Zylicz ◽  
Maud Borensztein ◽  
Frederick CK Wong ◽  
Yun Huang ◽  
Caroline Lee ◽  
...  
Keyword(s):  
Cell Fate ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Blastocyst Stage ◽  
Vital Role ◽  
Mouse Development ◽  
Cell Stage ◽  
Developmental Progression ◽  
Early Mouse ◽  
The Impact

Early mouse development is regulated and accompanied by dynamic changes in chromatin modifications, including G9a-mediated histone H3 lysine 9 dimethylation (H3K9me2). Previously, we provided insights into its role in post-implantation development (Zylicz et al., 2015). Here we explore the impact of depleting the maternally inherited G9a in oocytes on development shortly after fertilisation. We show that G9a accumulates typically at 4 to 8 cell stage to promote timely repression of a subset of 4 cell stage-specific genes. Loss of maternal inheritance of G9a disrupts the gene regulatory network resulting in developmental delay and destabilisation of inner cell mass lineages by the late blastocyst stage. Our results indicate a vital role of this maternally inherited epigenetic regulator in creating conducive conditions for developmental progression and on cell fate choices.

scholarly journals H3S10 Phosphorylation Marks Constitutive Heterochromatin During Interphase in Early Mouse Embryos Until the 4-Cell Stage

2012 ◽  
Vol 58 (4) ◽  
pp. 467-475 ◽  
Author(s):  
Karlla RIBEIRO-MASON ◽  
Claire BOULESTEIX ◽  
Renaud FLEUROT ◽  
Tiphaine AGUIRRE-LAVIN ◽  
Pierre ADENOT ◽  
...  
Keyword(s):  
Constitutive Heterochromatin ◽  
Mouse Embryos ◽  
Cell Stage ◽  
H3s10 Phosphorylation ◽  
Early Mouse

scholarly journals Profilin I is essential for cell survival and cell division in early mouse development

2001 ◽  
Vol 98 (7) ◽  
pp. 3832-3836 ◽  
Author(s):  
W. Witke ◽  
J. D. Sutherland ◽  
A. Sharpe ◽  
M. Arai ◽  
D. J. Kwiatkowski
Keyword(s):  
Cell Division ◽  
Cell Survival ◽  
Mouse Development ◽  
Early Mouse

Early transcription in Caenorhabditis elegans embryos

Development ◽  
1994 ◽  
Vol 120 (2) ◽  
pp. 443-451 ◽  
Author(s):  
L.G. Edgar ◽  
N. Wolf ◽  
W.B. Wood
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Cell Stage ◽  
Cell Cycles ◽  
Cell Lineages ◽  
C Elegans ◽  
Early Transcription ◽  
Alpha Amanitin ◽  
Autoradiographic Detection ◽  
Specific Timing

We have analysed early transcription in devitellinized, cultured embryos of the nematode Caenorhabditis elegans by two methods: measurement of [32P]UTP uptake into TCA-precipitable material and autoradiographic detection of [3H]UTP labelling both in the presence and absence of alpha-amanitin. RNA synthesis was first detected at the 8- to 12-cell stage, and alpha-amanitin sensitivity also appeared at this time, during the cleavages establishing the major founder cell lineages. The requirements for maternally supplied versus embryonically produced gene products in early embryogenesis were examined in the same culture system by observing the effects of alpha-amanitin on cell division and the early stereotyped lineage patterns. In the presence of high levels of alpha-amanitin added at varying times from two cells onward, cell division continued until approximately the 100-cell stage and then stopped during a single round of cell division. The characteristic unequal early cleavages, orientation of cleavage planes and lineage-specific timing of early divisions were unaffected by alpha-amanitin in embryos up to 87 cells. These results indicate that embryonic transcription starts well before gastrulation in C. elegans embryos, but that although embryonic transcripts may have important early functions, maternal products can support at least the mechanics of the first 6 to 7 cell cycles.

Glucose transporter gene expression in early mouse embryos

Development ◽  
1991 ◽  
Vol 113 (1) ◽  
pp. 363-372
Author(s):  
A. Hogan ◽  
S. Heyner ◽  
M.J. Charron ◽  
N.G. Copeland ◽  
D.J. Gilbert ◽  
...  
Keyword(s):  
Pancreatic Beta Cells ◽  
Glucose Transporter ◽  
Mouse Embryos ◽  
Preimplantation Development ◽  
Adult Brain ◽  
Chromosome 11 ◽  
Cell Stage ◽  
Glut 1 ◽  
Glut 4 ◽  
Early Mouse

The glucose transporter (GLUT) isoforms responsible for glucose uptake in early mouse embryos have been identified. GLUT 1, the isoform present in nearly every tissue examined including adult brain and erythrocytes, is expressed throughout preimplantation development. GLUT 2, which is normally present in adult liver, kidney, intestine and pancreatic beta cells is expressed from the 8-cell stage onward. GLUT 4, an insulin-recruitable isoform, which is expressed in adult fat and muscle, is not expressed at any stage of preimplantation development or in early postimplantation stage embryos. Genetic mapping studies of glucose transporters in the mouse show that Glut-1 is located on chromosome 4, Glut-2 on chromosome 3, Glut-3 on chromosome 6, and Glut-4 on chromosome 11.

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