The molecular basis of positional signalling: introduction

Development ◽  
1989 ◽  
Vol 107 (Supplement) ◽  
pp. 1-2
Author(s):  
R. R. Kay ◽  
J. C. Smith
Keyword(s):  
Molecular Biology ◽  
Embryonic Development ◽  
Sea Urchin ◽  
Molecular Basis ◽  
Normal Development ◽  
Cell Signalling ◽  
The Other ◽  
Embryonic Induction ◽  
Sea Urchin Embryo ◽  
Adjacent Group

The importance of cell–cell interactions in embryonic development was first described by Driesch (1891), who showed that any of the blastomeres of the 2-cell or 4-cell sea-urchin embryo is capable of forming a complete embryo if cultured in isolation; this implied that in normal development each blastomere is aware of the other and will only form a half- or quarter-embryo, as appropriate. And it was only ten years later that Spemann (1901) discovered the phenomenon of embryonic induction, recently reviewed by Gurdon (1987) and defined as an interaction in which the differentiation of one group of cells is affected by a signal from an adjacent group. Thus the significance of cell signalling during development has been appreciated for almost a century, but, as has frequently been remarked, progress in the molecular analysis of the phenomenon has been slow compared with that in the younger disciplines of, for example, immunology and molecular biology.

Molecular biology of the sea urchin embryo

Science ◽  
1982 ◽  
Vol 217 (4554) ◽  
pp. 17-26 ◽  
Author(s):  
E. Davidson ◽  
B. Hough-Evans ◽  
R. Britten
Keyword(s):  
Molecular Biology ◽  
Sea Urchin ◽  
Sea Urchin Embryo

scholarly journals The tolerance to hypoxia is defined by a time-sensitive response of the gene regulatory network in sea urchin embryos

2020 ◽  
Author(s):  
Majed Layous ◽  
Lama Khalaily ◽  
Tsvia Gildor ◽  
Smadar Ben-Tabou de-Leon
Keyword(s):  
Gene Regulatory Network ◽  
Early Development ◽  
Sea Urchin ◽  
Regulatory Network ◽  
Normal Development ◽  
Oxygen Level ◽  
Sea Urchin Embryo ◽  
Tolerance To Hypoxia ◽  
Vegf Pathway ◽  
Gene Regulatory

AbstractDeoxygenation, the reduction of oxygen level in the oceans induced by global warming and anthropogenic disturbances, is a major threat to marine life. This change in oxygen level could be especially harmful to marine embryos that utilize endogenous hypoxia and redox gradients as morphogens during normal development. Here we show that the tolerance to hypoxic conditions changes between different developmental stages of the sea urchin embryo, due to the structure of the gene regulatory networks (GRNs). We demonstrate that during normal development, bone morphogenetic protein (BMP) pathway restricts the activity of the vascular endothelial growth factor (VEGF) pathway to two lateral domains and by that controls proper skeletal patterning. Hypoxia applied during early development strongly perturbs the activity of Nodal and BMP pathways that affect VEGF pathway, dorsal-ventral (DV) and skeletogenic patterning. These pathways are largely unaffected by hypoxia applied after DV axis formation. We propose that the use of redox and hypoxia as morphogens makes the sea urchin embryo highly sensitive to environmental hypoxia during early development, but the GRN structure provides higher tolerance to hypoxia at later stages.Summary statementThe use of hypoxia and redox gradients as morphogens makes sea urchin early development sensitive to environmental hypoxia. This sensitivity decreases later, due to the structure of the gene regulatory network.

Purification and characterization of a 32-kDa protein that localizes to the sea urchin extraembryonic matrix, the hyaline layer

1992 ◽  
Vol 70 (8) ◽  
pp. 623-628 ◽  
Author(s):  
John J. Robinson
Keyword(s):  
Embryonic Development ◽  
Quantitative Determination ◽  
Sea Urchin ◽  
Polyclonal Antiserum ◽  
Purification And Characterization ◽  
Blastula Stage ◽  
Stage Of Development ◽  
Sea Urchin Egg ◽  
Sea Urchin Embryo

We have purified a 32 kilodalton (kDa) protein that localized with isolated, intact hyaline layers prepared from 1-h-old embryos. The protein appeared not to bind calcium and was not quantitatively released from 1-h-old embryos in the absence of Ca2+ and Mg2+. Using polyclonal antiserum prepared against the 32-kDa protein, the antigen was detected throughout embryonic development. By the hatched blastula stage of development, the 32-kDa protein was replaced by a species of slightly smaller molecular mass. Quantitative determination indicated that the 32-kDa protein accounted for approximately 6% of the total protein present in the sea urchin egg. This result is suggestive of a structural role for the 32-kDa protein that is required throughout embryonic development, although perhaps in a modified form from the hatched blastula stage on.Key words: sea urchin, embryo, hyaline layer, component.

scholarly journals Embryonic and post-embryonic utilization and subcellular localization of the nuclear receptor SpSHR2 in the sea urchin

1998 ◽  
Vol 111 (15) ◽  
pp. 2159-2169 ◽  
Author(s):  
A. Kontrogianni-Konstantopoulos ◽  
P.S. Leahy ◽  
C.N. Flytzanis
Keyword(s):  
Embryonic Development ◽  
Uniform Distribution ◽  
Nuclear Receptor ◽  
Sea Urchin ◽  
Embryonic Cells ◽  
Apical Position ◽  
Cell Stage ◽  
Maternal Rna ◽  
Sea Urchin Embryo ◽  
Pluteus Stage

SpSHR2 (Strongylocentrotus purpuratus steroid hormone receptor 2) is a nuclear receptor, encoded by a maternal RNA in the sea urchin embryo. These maternal SpSHR2 transcripts, which are present in all cells, persist until the blastula stage and then are rapidly turned over. A small fraction of the embryonic SpSHR2 protein is maternal, but the majority of this nuclear receptor in the embryo is the product of new synthesis, presumably from the maternal RNA after fertilization. In agreement with the mRNA distribution, the SpSHR2 protein is also detected in all embryonic cells. Contrary to the RNA though, the SpSHR2 protein persists throughout embryonic development to the pluteus stage, long after the mRNA is depleted. Following fertilization and as soon as the 2-cell stage, the cytoplasmic SpSHR2 protein enters rapidly into the embryonic nuclei where it appears in the form of speckles. During subsequent stages (from fourth cleavage onward), SpSHR2 resides in speckled form in both the nucleus and the cytoplasm of the embryonic cells. The cytoplasmic localization of SpSHR2 differs between polarized and non-polarized cells, maintaining an apical position in the ectoderm and endoderm versus a uniform distribution in mesenchyme cells. Following the end of embryonic development (pluteus stage), the SpSHR2 protein is depleted from all tissues. During the ensuing four weeks of larval development, the SpSHR2 is not detected in either the larval or the rudiment cells which will give rise to the adult. Just prior to metamorphosis, at about 35 days post-fertilization, the protein is detected again but in contrast to the uniform distribution in the early embryo, the larval SpSHR2 is specifically expressed in cells of the mouth epithelium and the epaulettes. In adult ovaries and testes, SpSHR2 is specifically detected in the myoepithelial cells surrounding the ovarioles and the testicular acini. Nuclear SpSHR2 in blastula extracts binds to the C1R hormone response element in the upstream promoter region of the CyIIIb actin gene indicating that the latter may be a target of this nuclear receptor in the sea urchin embryo.

scholarly journals The tolerance to hypoxia is defined by a time-sensitive response of the gene regulatory network in sea urchin embryos

Development ◽  
2021 ◽  
pp. dev.195859
Author(s):  
Majed Layous ◽  
Lama Khalaily ◽  
Tsvia Gildor ◽  
Smadar Ben-Tabou de-Leon
Keyword(s):  
Early Development ◽  
Sea Urchin ◽  
Regulatory Networks ◽  
Normal Development ◽  
Axis Formation ◽  
Oxygen Level ◽  
Sea Urchin Embryo ◽  
Tolerance To Hypoxia ◽  
Vegf Pathway ◽  
Gene Regulatory

Deoxygenation, the reduction of oxygen level in the oceans induced by global warming and anthropogenic disturbances, is a major threat to marine life. This change in oxygen level could be especially harmful to marine embryos that utilize endogenous hypoxia and redox gradients as morphogens during normal development. Here we show that the tolerance to hypoxic conditions changes between different developmental stages of the sea urchin embryo, possibly due to the structure of the gene regulatory networks (GRNs). We demonstrate that during normal development, bone morphogenetic protein (BMP) pathway restricts the activity of the vascular endothelial growth factor (VEGF) pathway to two lateral domains and by that controls proper skeletal patterning. Hypoxia applied during early development strongly perturbs the activity of Nodal and BMP pathways that affect VEGF pathway, dorsal-ventral (DV) and skeletogenic patterning. These pathways are largely unaffected by hypoxia applied after DV-axis formation. We propose that the use of redox and hypoxia as morphogens makes the sea urchin embryo highly sensitive to environmental hypoxia during early development, but the GRN structure provides higher tolerance to hypoxia at later stages.

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