Early cell fate decisions in the mouse embryo

Saiz, Néstor; Płusa, Berenika

doi:10.1530/rep-12-0381

Cited by 89 publications

(82 citation statements)

References 162 publications

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“…The TE mediates implantation of the embryo into the uterus and placenta formation for further maternal sustenance of embryonic development. The PrE develops into the visceral endoderm (VE) and the parietal endoderm (ParE) after implantation [7–9] (Fig. 1).…”

Section: The Developmental Origin Of Escsmentioning

confidence: 99%

Molecular basis of embryonic stem cell self-renewal: from signaling pathways to pluripotency network

Huang

Zhou

et al. 2015

Cell. Mol. Life Sci.

127

113

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Embryonic stem cells (ESCs) can be maintained in culture indefinitely while retaining the capacity to generate any type of cell in the body, and therefore not only hold great promise for tissue repair and regeneration, but also provide a powerful tool for modeling human disease and understanding biological development. In order to fulfill the full potential of ESCs, it is critical to understand how ESC fate, whether to self-renew or to differentiate into specialized cells, is regulated. On the molecular level, ESC fate is controlled by the intracellular transcriptional regulatory networks that respond to various extrinsic signaling stimuli. In this review, we discuss and compare important signaling pathways in the self-renewal and differentiation of mouse, rat, and human ESCs with an emphasis on how these pathways integrate into ESC-specific transcription circuitries. This will be beneficial for understanding the common and conserved mechanisms that govern self-renewal, and for developing novel culture conditions that support ESC derivation and maintenance.

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Section: The Developmental Origin Of Escsmentioning

confidence: 99%

Molecular basis of embryonic stem cell self-renewal: from signaling pathways to pluripotency network

Huang

Zhou

et al. 2015

Cell. Mol. Life Sci.

127

113

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“…Three divisions after fertilization, the 8-cell mouse embryo initiates two morphogenetic processes: compaction and polarization (Saiz and Plusa, 2013;Yamanaka et al, 2006). Compaction minimizes embryo surface area and polarization establishes apico-basal cell polarity in each blastomere.…”

Section: Introductionmentioning

confidence: 99%

Initiation of Hippo signaling is linked to polarity rather than to cell position in the pre-implantation mouse embryo

et al. 2014

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In the mouse embryo, asymmetric divisions during the 8-16 cell division generate two cell types, polar and apolar cells, that are allocated to outer and inner positions, respectively. This outer/inner configuration is the first sign of the formation of the first two cell lineages: trophectoderm (TE) and inner cell mass (ICM). Outer polar cells become TE and give rise to the placenta, whereas inner apolar cells become ICM and give rise to the embryo proper and yolk sac. Here, we analyze the frequency of asymmetric divisions during the 8-16 cell division and assess the relationships between cell polarity, cell and nuclear position, and Hippo signaling activation, the pathway that initiates lineage-specific gene expression in 16-cell embryos. Although the frequency of asymmetric divisions varied in each embryo, we found that more than six blastomeres divided asymmetrically in most embryos. Interestingly, many apolar cells in 16-cell embryos were located at outer positions, whereas only one or two apolar cells were located at inner positions. Live imaging analysis showed that outer apolar cells were eventually internalized by surrounding polar cells. Using isolated 8-cell blastomeres, we carefully analyzed the internalization process of apolar cells and found indications of higher cortical tension in apolar cells than in polar cells. Last, we found that apolar cells activate Hippo signaling prior to taking inner positions. Our results suggest that polar and apolar cells have intrinsic differences that establish outer/inner configuration and differentially regulate Hippo signaling to activate lineage-specific gene expression programs.

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“…Pictures were taken at the 96th h of culture and embryos were classified based on the expansion of blastocoel [early and mid-, expanded and hatched blastocysts (Saiz and Plusa, 2013)]. …”

Section: Embryo Culture and Treatmentmentioning

confidence: 99%

T-2 mycotoxin slows down the development of mouse blastocysts, decreases their blastomere number and increases chromatin damage

Somoskői

Kovács

Cseh

2016

Acta Veterinaria Hungarica

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The mycotoxin T-2 has many harmful effects on mammalian cells and reproductive functions. In the present study, the in vitro effect of T-2 toxin on mouse blastocysts was examined. Embryos were cultured in media supplemented with 0.5, 0.75 and 1 ng/ml T-2. Different exposure times were applied [96 h (treatment I) or 24 h following 72 h in toxin-free media (treatment II)]. Blastomere number, nuclear chromatin status and blastocoel formation were investigated in blastocysts. Our data show that the effect of T-2 toxin may vary depending on the stage of the embryo at the start of exposure. At 96 h of exposure, the blastocysts had blastomeres with normal chromatin quality but their developmental potential was decreased. After 24 h of exposure applied following a 72-h culture, blastomeres had a higher level of chromatin damage, although their developmental potential was the same as in the control embryos. In both cases, decreased mitotic rate was found, which resulted in decreased blastomere number even at low toxin concentration.

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Early cell fate decisions in the mouse embryo

Cited by 89 publications

References 162 publications

Molecular basis of embryonic stem cell self-renewal: from signaling pathways to pluripotency network

Molecular basis of embryonic stem cell self-renewal: from signaling pathways to pluripotency network

Initiation of Hippo signaling is linked to polarity rather than to cell position in the pre-implantation mouse embryo

T-2 mycotoxin slows down the development of mouse blastocysts, decreases their blastomere number and increases chromatin damage

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