The establishment of the embryonic-abembryonic axis in the mouse embryo

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 125-134 ◽  
Author(s):  
C.L. Garbutt ◽  
J.C. Chisholm ◽  
M.H. Johnson
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Blastocyst Stage ◽  
Dividing Cells ◽  
Intercellular Cooperation

The influence of cell division order on the establishment of the embryonic-abembryonic axis (EA axis) of the mouse embryo was investigated. Aggregate embryos were constructed in which a labelled cell (or pair of cells) was combined with a group of unlabelled cells all of which were up to one cell cycle earlier or later in their progress through development to the blastocyst stage. The aggregates were cultured first to the nascent blastocyst stage and then to the expanded blastocyst stage. The positions of the progeny of the labelled cells in relation to the nascent blastocoel and to the orientation of the embryonic-abembryonic axis were recorded. It was concluded that cell division order does influence the establishment of the EA axis, early dividing cells tending to be associated with the nascent blastocoel and the site of the nascent blastocoel tending to mark the site of the abembryonic pole. However, the influence of division order was diminished by a requirement for intercellular cooperation during blastocoel formation and by a counteracting influence of division order arising from its effects on the allocation of cells to the inner cell mass.

Gp330 is specifically expressed in outer cells during epithelial differentiation in the preimplantation mouse embryo

Development ◽  
1994 ◽  
Vol 120 (11) ◽  
pp. 3289-3299 ◽  
Author(s):  
C. Gueth-Hallonet ◽  
A. Santa-Maria ◽  
P. Verroust ◽  
B. Maro
Keyword(s):  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Blastocyst Stage ◽  
Transcriptional Level ◽  
Cell Stage ◽  
Preimplantation Mouse ◽  
Extensive Cell ◽  
High Level ◽  
Endocytic Activity

During preimplantation development of the mouse embryo, a layer of outer cells differentiates into a perfect epithelium, the trophectoderm. The divergence between the trophectoderm and the inner cell mass takes place from the 8-cell stage to the 64-cell stage and precedes their commitment at the blastocyst stage. In this work, we have investigated the expression of gp330, a 330 × 10(3) M(r) glycoprotein found in clathrin-coated areas of the plasma membrane of some epithelial cells characterized by a high level of endocytic activity. Our results show that gp330 is first synthesized in 16-cell stage embryos and that its appearance is restricted to outer cells until the blastocyst stage. Furthermore, its expression is repressed in inner cells at a post-transcriptional level, probably through the development of extensive cell-cell contacts.

Cytokeratin filament assembly in the preimplantation mouse embryo

Development ◽  
1987 ◽  
Vol 101 (3) ◽  
pp. 565-582 ◽  
Author(s):  
J.C. Chisholm ◽  
E. Houliston
Keyword(s):  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Blastocyst Stage ◽  
Lineage Tracing ◽  
Cell Stage ◽  
Filament Assembly ◽  
Filament Networks ◽  
Tracing Techniques ◽  
Cytokeratin Filaments

The timing, spatial distribution and control of cytokeratin assembly during mouse early development has been studied using a monoclonal antibody, TROMA-1, which recognizes a 55,000 Mr trophectodermal cytokeratin (ENDO A). This protein was first detected in immunoblots at the 4-cell stage, and became more abundant at the 16-cell stage and later. Immunofluorescence analysis revealed assembled cytokeratin filaments in some 8-cell blastomeres, but not at earlier stages. At the 16-cell stage, filaments were found in both polarized (presumptive trophectoderm; TE) and apolar (presumptive inner cell mass; ICM) cells in similar proportions, although polarized cells possessed more filaments than apolar cells. By the late 32-cell, early blastocyst, stage, all polarized (TE) cells contained extensive filament networks whereas cells positioned inside the embryo tended to have lost their filaments. The presence of filaments in inside cells at the 16-cell stage and in ICM cells was confirmed by immunoelectron microscopy. Lineage tracing techniques demonstrated that those cells in the ICM of early blastocysts which did possess filaments were almost exclusively the progeny of polar 16-cell blastomeres, suggesting that these filaments were directly inherited from outside cells at the 16- to 32-cell transition. Inhibitor studies revealed that proximate protein synthesis but not mRNA synthesis is required for filament assembly at the 8-cell stage. These results demonstrate that there are quantitative rather than qualitative differences in the expression of cytokeratin filaments in the inner cell mass and trophectoderm cells of the mouse embryo.

Actin nucleator Arp2/3 complex is essential for mouse preimplantation embryo development

2013 ◽  
Vol 25 (4) ◽  
pp. 617 ◽  
Author(s):  
Shao-Chen Sun ◽  
Qing-Ling Wang ◽  
Wei-Wei Gao ◽  
Yong-Nan Xu ◽  
Hong-Lin Liu ◽  
...  
Keyword(s):  
Cell Division ◽  
Embryo Development ◽  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Specific Inhibitor ◽  
Cell Stage ◽  
Diverse Range ◽  
Mouse Embryo Development ◽  
Actin Nucleator

The Arp2/3 complex is a critical actin nucleator, which promotes actin assembly and is widely involved in a diverse range of actin-related processes such as cell locomotion, phagocytosis and the establishment of cell polarity. Previous studies showed that the Arp2/3 complex regulates spindle migration and asymmetric division during mouse oocyte maturation; however, the role of the Arp2/3 complex in early mouse embryo development is still unknown. The results of the present study show that the Arp2/3 complex is critical for cytokinesis during mouse embryo development. The Arp2/3 complex was concentrated at the cortex of each cell at the 2- to 8-cell stage and the peripheral areas of the morula and blastocyst. Inhibition of the Arp2/3 complex by the specific inhibitor CK666 at the zygote stage caused a failure in cell division; mouse embryos failed to undergo compaction and lost apical–basal polarity. The actin level decreased in the CK666-treated group, and two or more nuclei were observed within a single cell, indicating a failure of cell division. Addition of CK666 at the 8-cell stage caused a failure of blastocyst formation, and CDX2 staining confirmed the loss of embryo polarity and the failure of trophectoderm and inner cell mass formation. Taken together, these data suggest that the Arp2/3 complex may regulate mouse embryo development via its effect on cell division.

Experimental studies on the organization of the preimplantation mouse embryo

Development ◽  
1972 ◽  
Vol 28 (2) ◽  
pp. 247-254
Author(s):  
M. Susan Stern ◽  
I. B. Wilson
Keyword(s):  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Experimental Studies ◽  
Blastocyst Stage ◽  
Stages Of Development ◽  
Preimplantation Mouse Embryo ◽  
Different Ages ◽  
Preimplantation Mouse ◽  
Mouse Eggs

The interaction between mouse eggs conjoined in pairs of different ages and stages of development has been examined: 1. Forty-two per cent of chimaeras formed from 8-cell eggs paired with late morulae or early blastocysts produced morphologically normal, but large, blastocysts. 2. Fusion of pairs of vitally labelled and unlabelled eggs has shown that presumptive trophoblast derived from as late as the early blastocyst stage can become incorporated into the inner cell mass of chimaeras. These observations suggest that the preimplantation chimaeric embryo can regulate for chronological differences in its constituent cells and that the trophoblast up to the early blastocyst stage may still be developmentally labile.

scholarly journals A general quantitative relation linking bacterial cell growth and the cell cycle

2019 ◽  
Author(s):  
Hai Zheng ◽  
Yang Bai ◽  
Meiling Jiang ◽  
Taku A. Tokuyasu ◽  
Xiongliang Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Cell Division ◽  
Bacterial Cell ◽  
Cell Mass ◽  
Quantitative Relation ◽  
Growth Physiology ◽  
Dividing Cells ◽  
Bacterial Cell Cycle ◽  
Doubling Times

The foundation of bacterial cell cycle studies has long resided in two interconnected dogmas between biomass growth, DNA replication, and cell division during exponential growth: the SMK growth law that relates cell mass (a measure of cell size) to growth rate1, and Donachie’s hypothesis of a growth-rate-independent initiation mass2. These dogmas have spurred many efforts to understand their molecular bases and physiological consequences3–12. Most of these studies focused on fast-growing cells, with doubling times shorter than 60 min. Here, we systematically studied the cell cycle of E. coli for a broad range of doubling times (24 min to over 10 hr), with particular attention on steady-state growth. Surprisingly, we observed that neither dogma held across the range of growth rates examined. In their stead, a new linear relation unifying the slow- and fast-growth regimes was revealed between the cell mass and the number of cell divisions it takes to replicate and segregate a newly initiated pair of replication origins. This and other findings in this study suggest a single-cell division model, which not only reproduces the bulk relations observed but also recapitulates the adder phenomenon established recently for stochastically dividing cells13–15. These results allowed us to develop quantitative insight into the bacterial cell cycle, providing a firm new foundation for the study of bacterial growth physiology.

scholarly journals Aberrant cell cycle checkpoint function and early embryonic death in Chk1−/− mice

2000 ◽  
Vol 14 (12) ◽  
pp. 1439-1447 ◽  
Author(s):  
Hiroyuki Takai ◽  
Kaoru Tominaga ◽  
Noboru Motoyama ◽  
Yohji A. Minamishima ◽  
Hiroyasu Nagahama ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Blastocyst Stage ◽  
Cell Cycle Checkpoint ◽  
Targeted Disruption ◽  
Checkpoint Kinases ◽  
Cycle Checkpoint ◽  
Replication Block

The recent discovery of checkpoint kinases has suggested the conservation of checkpoint mechanisms between yeast and mammals. In yeast, the protein kinase Chk1 is thought to mediate signaling associated with the DNA damage checkpoint of the cell cycle. However, the function of Chk1 in mammals has remained unknown. Targeted disruption of Chk1 in mice showed thatChk1−/− embryos exhibit gross morphologic abnormalities in nuclei as early as the blastocyst stage. In culture, Chk1−/− blastocysts showed a severe defect in outgrowth of the inner cell mass and died of apoptosis. DNA replication block and DNA damage failed to arrest the cell cycle before initiation of mitosis inChk1−/− embryos. These results may indicate that Chk1 is indispensable for cell proliferation and survival through maintaining the G2 checkpoint in mammals.

scholarly journals Establishing the Initial Embryonic Axis

2007 ◽  
Vol 15 (6) ◽  
pp. 3-5
Author(s):  
Stephen W. Carmichael ◽  
Gary C. Schoenwolf
Keyword(s):  
Cell Division ◽  
Mouse Model ◽  
Inner Cell Mass ◽  
Molecular Genetic ◽  
Cell Mass ◽  
Embryonic Axis ◽  
The Other ◽  
Mammalian Embryo ◽  
Cell Divisions ◽  
Dividing Cells

In the mammalian embryo, the first axis to appear is at the time of the fifth cell division when the inner cell mass (ICM) becomes visible. The localization of the ICM on one side of a cavity formed within the cluster of dividing cells marks the embryonic-abembryonic (E-Ab) axis. This name derives from the fact the most of the embryo will develop from the ICM, whereas other tissues (the placenta, etc.) will develop from the other cells. There has been a long-standing controversy as to what determines the mammalian E-Ab axis; is the information inherently in the zygote, or is it determined after several cell divisions? In an elegant series of studies whereby dividing cells were labeled using new molecular genetic tools and then carefully followed during development, Yoko Kurotaki, Kohei Hatta, Kazuki Nakao, Yo-ichi Nabeshima, and Toshihiko Fujimori have provided an answer in a mouse model.

Use of F9 teratocarcinoma STEM cells to study cell-matrix interactions in the early mouse embryo

1992 ◽  
Vol 50 (1) ◽  
pp. 602-603
Author(s):  
Marc Lenburg ◽  
Rulang Jiang ◽  
Lengya Cheng ◽  
Laura Grabel
Keyword(s):  
Mouse Embryo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Types ◽  
Embryoid Bodies ◽  
F9 Cells ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions ◽  
F9 Teratocarcinoma

We are interested in defining the cell-cell and cell-matrix interactions that help direct the differentiation of extraembryonic endoderm in the peri-implantation mouse embryo. At the blastocyst stage the mouse embryo consists of an outer layer of trophectoderm surrounding the fluid-filled blastocoel cavity and an eccentrically located inner cell mass. On the free surface of the inner cell mass, facing the blastocoel cavity, a layer of primitive endoderm forms. Primitive endoderm then generates two distinct cell types; parietal endoderm (PE) which migrates along the inner surface of the trophectoderm and secretes large amounts of basement membrane components as well as tissue-type plasminogen activator (tPA), and visceral endoderm (VE), a columnar epithelial layer characterized by tight junctions, microvilli, and the synthesis and secretion of α-fetoprotein. As these events occur after implantation, we have turned to the F9 teratocarcinoma system as an in vitro model for examining the differentiation of these cell types. When F9 cells are treated in monolayer with retinoic acid plus cyclic-AMP, they differentiate into PE. In contrast, when F9 cells are treated in suspension with retinoic acid, they form embryoid bodies (EBs) which consist of an outer layer of VE and an inner core of undifferentiated stem cells. In addition, we have established that when VE containing embryoid bodies are plated on a fibronectin coated substrate, PE migrates onto the matrix and this interaction is inhibited by RGDS as well as antibodies directed against the β1 integrin subunit. This transition is accompanied by a significant increase in the level of tPA in the PE cells. Thus, the outgrowth system provides a spatially appropriate model for studying the differentiation and migration of PE from a VE precursor.

scholarly journals Cell fate clusters in ICM organoids arise from cell fate heredity and division: a modelling approach

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tim Liebisch ◽  
Armin Drusko ◽  
Biena Mathew ◽  
Ernst H. K. Stelzer ◽  
Sabine C. Fischer ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Cell Fate ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Lineage ◽  
Cell Fate Decision ◽  
Cell Fate Decisions ◽  
Chemical Signalling ◽  
Fate Decision

AbstractDuring the mammalian preimplantation phase, cells undergo two subsequent cell fate decisions. During the first decision, the trophectoderm and the inner cell mass are formed. Subsequently, the inner cell mass segregates into the epiblast and the primitive endoderm. Inner cell mass organoids represent an experimental model system, mimicking the second cell fate decision. It has been shown that cells of the same fate tend to cluster stronger than expected for random cell fate decisions. Three major processes are hypothesised to contribute to the cell fate arrangements: (1) chemical signalling; (2) cell sorting; and (3) cell proliferation. In order to quantify the influence of cell proliferation on the observed cell lineage type clustering, we developed an agent-based model accounting for mechanical cell–cell interaction, i.e. adhesion and repulsion, cell division, stochastic cell fate decision and cell fate heredity. The model supports the hypothesis that initial cell fate acquisition is a stochastically driven process, taking place in the early development of inner cell mass organoids. Further, we show that the observed neighbourhood structures can emerge solely due to cell fate heredity during cell division.

scholarly journals Position- and Hippo signaling-dependent plasticity during lineage segregation in the early mouse embryo

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Eszter Posfai ◽  
Sophie Petropoulos ◽  
Flavia Regina Oliveira de Barros ◽  
John Paul Schell ◽  
Igor Jurisica ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Global Gene Expression ◽  
Blastocyst Stage ◽  
Egfp Expression ◽  
Hippo Signaling ◽  
Ability To Regenerate ◽  
Early Mouse ◽  
Cell Commitment

The segregation of the trophectoderm (TE) from the inner cell mass (ICM) in the mouse blastocyst is determined by position-dependent Hippo signaling. However, the window of responsiveness to Hippo signaling, the exact timing of lineage commitment and the overall relationship between cell commitment and global gene expression changes are still unclear. Single-cell RNA sequencing during lineage segregation revealed that the TE transcriptional profile stabilizes earlier than the ICM and prior to blastocyst formation. Using quantitative Cdx2-eGFP expression as a readout of Hippo signaling activity, we assessed the experimental potential of individual blastomeres based on their level of Cdx2-eGFP expression and correlated potential with gene expression dynamics. We find that TE specification and commitment coincide and occur at the time of transcriptional stabilization, whereas ICM cells still retain the ability to regenerate TE up to the early blastocyst stage. Plasticity of both lineages is coincident with their window of sensitivity to Hippo signaling.

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