scholarly journals cis-Regulatory sequences driving the expression of the Hbox12 homeobox-containing gene in the presumptive aboral ectoderm territory of the Paracentrotus lividus sea urchin embryo

2008 ◽  
Vol 321 (2) ◽  
pp. 455-469 ◽  
Author(s):  
Vincenzo Cavalieri ◽  
Maria Di Bernardo ◽  
Letizia Anello ◽  
Giovanni Spinelli
Keyword(s):  
Sea Urchin ◽  
Paracentrotus Lividus ◽  
Regulatory Sequences ◽  
Sea Urchin Embryo

Cell junctions during the early development of the sea urchin embryo (Paracentrotus lividus)

1987 ◽  
Vol 20 (2-3) ◽  
pp. 137-146 ◽  
Author(s):  
P. Andreuccetti ◽  
M.R. Barone Lumaga ◽  
G. Cafiero ◽  
S. Filosa ◽  
E. Parisi
Keyword(s):  
Early Development ◽  
Sea Urchin ◽  
Paracentrotus Lividus ◽  
Cell Junctions ◽  
Sea Urchin Embryo

scholarly journals Early asymmetric cues triggering the dorsal/ventral gene regulatory network of the sea urchin embryo

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Vincenzo Cavalieri ◽  
Giovanni Spinelli
Keyword(s):  
Gene Regulatory Network ◽  
Sea Urchin ◽  
Regulatory Network ◽  
Ectopic Expression ◽  
Paracentrotus Lividus ◽  
Loss Of Function ◽  
Mapk Activity ◽  
Sea Urchin Embryo ◽  
Gene Regulatory ◽  
Dorsal Cells

Dorsal/ventral (DV) patterning of the sea urchin embryo relies on a ventrally-localized organizer expressing Nodal, a pivotal regulator of the DV gene regulatory network. However, the inceptive mechanisms imposing the symmetry-breaking are incompletely understood. In Paracentrotus lividus, the Hbox12 homeodomain-containing repressor is expressed by prospective dorsal cells, spatially facing and preceding the onset of nodal transcription. We report that Hbox12 misexpression provokes DV abnormalities, attenuating nodal and nodal-dependent transcription. Reciprocally, impairing hbox12 function disrupts DV polarity by allowing ectopic expression of nodal. Clonal loss-of-function, inflicted by blastomere transplantation or gene-transfer assays, highlights that DV polarization requires Hbox12 action in dorsal cells. Remarkably, the localized knock-down of nodal restores DV polarity of embryos lacking hbox12 function. Finally, we show that hbox12 is a dorsal-specific negative modulator of the p38-MAPK activity, which is required for nodal expression. Altogether, our results suggest that Hbox12 function is essential for proper positioning of the DV organizer.

Ectoderm-ECM signaling promotes skeletal growth in the Paracentrotus lividus sea urchin embryo

2004 ◽  
pp. 83-87
Author(s):  
R Russo ◽  
V Matranga ◽  
F Zito ◽  
C Costa ◽  
S Sciarrino ◽  
...  
Keyword(s):  
Sea Urchin ◽  
Paracentrotus Lividus ◽  
Skeletal Growth ◽  
Sea Urchin Embryo

scholarly journals Evidence for MAP kinase activation during mitotic division

1998 ◽  
Vol 111 (17) ◽  
pp. 2519-2527 ◽  
Author(s):  
S. Chiri ◽  
C. De Nadai ◽  
B. Ciapa
Keyword(s):  
Map Kinase ◽  
Sea Urchin ◽  
Map Kinases ◽  
Kinase Activity ◽  
Paracentrotus Lividus ◽  
Mitotic Division ◽  
Quiescent State ◽  
Kinase Activation ◽  
Cellular Events ◽  
Sea Urchin Embryo

MAP kinases have been implicated in the control of a broad spectrum of cellular events in many types of cells. In somatic cells, MAP kinase activation seems to be triggered after exit from a quiescent state (in G0 or G2) only and then inactivated by entry into a proliferative state. In oocytes of various species, a one-time activation of MAP kinase that is apparently not repeated during the succeeding mitotic cycles occurs after meiotic activation. However, several reports suggest that a myelin basic protein (MBP) kinase activity, unrelated to that of maturation promoting factor, can sometimes be detected during mitotic divisions in various types of cells and oocytes. We have reinvestigated this problem in order to determine the origin and the role of MBP kinase that is stimulated at time of mitosis in the fertilized eggs of the sea urchin Paracentrotus lividus. We used anti-ERK1 antibodies or substrates specific for different MAP kinases, and performed in-gel phosphorylation experiments. Our results suggest that an ERK1-like protein was responsible for part of the MBP kinase activity that is stimulated during the first mitotic divisions. Furthermore, we observed that wortmannin, an inhibitor of PI 3-kinase that arrests the fertilized sea urchin eggs at the prometaphase stage, inhibited the inactivation of MAP kinase normally observed when the eggs divide, suggesting a role for PI 3-kinase in the deactivation process of MAP kinase. We also discuss how the activities of MPF and MAP kinase may be interconnected to regulate the first mitotic divisions of the early sea urchin embryo.

scholarly journals Differential stability of expression of similarly specified endogenous and exogenous genes in the sea urchin embryo

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 385-398 ◽  
Author(s):  
D.L. Livant ◽  
B.R. Hough-Evans ◽  
J.G. Moore ◽  
R.J. Britten ◽  
E.H. Davidson
Keyword(s):  
Sea Urchin ◽  
Protein Interactions ◽  
Fusion Gene ◽  
Regulatory Sequences ◽  
Mrna Levels ◽  
Dna Fragments ◽  
Exogenous Dna ◽  
Sea Urchin Embryo ◽  
Regulatory Dna

The object of these experiments was to determine whether competitive titration in vivo of factors required for expression of the CyIIIa.CAT fusion gene would affect expression of the endogenous CyIIIa gene in the same embryos. Earlier work showed that expression of this fusion gene after injection into sea urchin eggs is stoichiometrically reduced when low molar excesses of DNA fragments containing only its regulatory domain are coinjected. In order to compare endogenous (i.e. CyIIIa) and exogenous (i.e. CyIIIa.CAT) expression simultaneously in embryos bearing excess competitor regulatory DNA, we developed, and here describe, a new procedure for generating transgenic sea urchin embryos in which all of the cells in many embryos, and most in others, bear the exogenous DNA. Such large reduction of mosaicism can be achieved by multiple injection of the exogenous DNA fragments into fertilized eggs. Using this method, we demonstrate that at a level of competitor DNA incorporation which reduces CyIIIa.CAT expression by 85%, endogenous CyIIIa mRNA levels are wholly unaffected. Nor is spatial expression of the endogenous CyIIIa gene disturbed. Since the CyIIIa.CAT genes are properly expressed under control of the CyIIIa regulatory sequences, they must participate in the same set of necessary DNA-protein interactions. However, we infer from the results that we report here that the regulatory complexes in the endogenous CyIIIa gene are greatly stabilized relative to those of the exogenous CyIIIa.CAT genes.

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