Sea Urchin Development (sea + urchin_development)

Distribution by Scientific Domains


Selected Abstracts


Blocking Dishevelled signaling in the noncanonical Wnt pathway in sea urchins disrupts endoderm formation and spiculogenesis, but not secondary mesoderm formation

DEVELOPMENTAL DYNAMICS, Issue 7 2009
Christine A. Byrum
Abstract Dishevelled (Dsh) is a phosphoprotein key to beta-catenin dependent (canonical) and beta-catenin independent (noncanonical) Wnt signaling. Whereas canonical Wnt signaling has been intensively studied in sea urchin development, little is known about other Wnt pathways. To examine roles of these beta-catenin independent pathways in embryogenesis, we used Dsh-DEP, a deletion construct blocking planar cell polarity (PCP) and Wnt/Ca2+ signaling. Embryos overexpressing Dsh-DEP failed to gastrulate or undergo skeletogenesis, but produced pigment cells. Although early mesodermal gene expression was largely unperturbed, embryos exhibited reduced expression of genes regulating endoderm specification and differentiation. Overexpressing activated beta-catenin failed to rescue Dsh-DEP embryos, indicating that Dsh-DEP blocks endoderm formation downstream of initial canonical Wnt signaling. Because Dsh-DEP-like constructs block PCP signaling in other metazoans, and disrupting RhoA or Fz 5/8 in echinoids blocks subsets of the Dsh-DEP phenotypes, our data suggest that noncanonical Wnt signaling is crucial for sea urchin endoderm formation and skeletogenesis. Developmental Dynamics 238:1649,1665, 2009. © 2009 Wiley-Liss, Inc. [source]


Genes involved in the RNA interference pathway are differentially expressed during sea urchin development

DEVELOPMENTAL DYNAMICS, Issue 11 2007
Jia L. Song
Abstract RNA-mediated interference (RNAi) is a conserved gene silencing mechanism that involves double-stranded RNA as a signal to trigger the sequence-specific degradation of target mRNA, resulting in posttranscriptional silencing and/or translational repression. Bioinformatic searches in the sea urchin genome database identified homologs of Drosha, DGCR5, Dicer, TRBP, Exportin-5, and Argonautes. Quantitative, real-time polymerase chain reaction indicated that all mRNA accumulate in eggs and in variable levels throughout early development. Whole-mount in situ RNA hybridization showed that all of the important players of the RNAi silencing pathway have abundant mRNA accumulation in oocytes and eggs, but have distinct spatial and temporal expression patterns throughout development. Sequence analysis revealed that each of the four Argonautes examined contain conserved residues important for RNAseH activity within the Piwi domain. This study elucidated that genes involved in the RNAi silencing pathway have dynamic expression and, thus, may have regulatory roles during germ cell development and embryogenesis. Developmental Dynamics 236:3180,3190, 2007. © 2007 Wiley-Liss, Inc. [source]


Morphological evolution in sea urchin development: hybrids provide insights into the pace of evolution

BIOESSAYS, Issue 4 2004
Maria Byrne
Hybridisations between related species with divergent ontogenies can provide insights into the bases for evolutionary change in development. One example of such hybridisations involves sea urchin species that exhibit either standard larval (pluteal) stages or those that develop directly from embryo to adult without an intervening feeding larval stage. In such crosses, pluteal features were found to be restored in fertilisations of the eggs of some direct developing sea urchins (Heliocidaris erythrogramma) with the sperm of closely (Heliocidaris tuberculata) and distantly (Pseudoboletia maculata) related species with feeding larvae. Such results can be argued to support the punctuated equilibrium model,conservation in pluteal regulatory systems and a comparatively rapid switch to direct development in evolution.1,2 Generation of hybrids between distantly related direct developers may, however, indicate evolutionary convergence. The ,rescue' of pluteal features by paternal genomes may require maternal factors from H. erythrogramma because the larva of this species has pluteal features. In contrast, pluteal features were not restored in hybridisations with the eggs of Holopneustes purpurescens, which lacks pluteal features. How much of pluteal development can be lost before it cannot be rescued in such crosses? The answer awaits hybridisations among indirect and direct developing sea urchins differing in developmental phenotype, in parallel with investigations of the genetic programs involved. BioEssays 26:343,347, 2004. © 2004 Wiley Periodicals, Inc. [source]


The modulator is a constitutive enhancer of a developmentally regulated sea urchin histone H2A gene

BIOESSAYS, Issue 9 2002
Giovanni Spinelli
Going back to the late 1970s and early 1980s, we trace the Xenopus oocyte microinjection experiments that led to the emergence of the concept of "modulator". The finding that the modulator could transactivate transcription from far upstream and in either orientation suggested that a new genetic element, different from the classical prokaryotic promoter sequences, had been discovered. This particular enhancer transactivates transcription of the sea urchin early (,) histone H2A gene which is regulated in early sea urchin development. We summarise the data from sea urchin microinjection experiments that confirm and extend the results obtained with Xenopus oocytes. We conclude that the H2A enhancer is bipartite, is located approx. 100 bp upstream of the TATAAATA box in the H2A gene of two sea urchin species and enhances transcription when placed at a position far upstream or far downstream of the gene unless an insulator intervenes between enhancer and promoter. Evidence from microinjection experiments with sea urchin embryos suggests that the developmental control of H2A expression resides not with the enhancer, which is constitutively active, but with a striking chromatin structure with two positioned nucleosomes near the 3, end of the gene. Within this structure, there is an insulator element. BioEssays 24:850,857, 2002. © 2002 Wiley Periodicals, Inc. [source]