scholarly journals Expression of Pigment Cell-Specific Genes in the Ontogenesis of the Sea UrchinStrongylocentrotus intermedius

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Natalya V. Ageenko ◽  
Konstantin V. Kiselev ◽  
Nelly A. Odintsova

One of the polyketide compounds, the naphthoquinone pigment echinochrome, is synthesized in sea urchin pigment cells. We analyzed polyketide synthase (pks) and sulfotransferase (sult) gene expression in embryos and larvae of the sea urchinStrongylocentrotus intermediusfrom various stages of development and in specific tissues of the adults. We observed the highest level of expression of thepksandsultgenes at the gastrula stage. In unfertilized eggs, only trace amounts of thepksandsulttranscripts were detected, whereas no transcripts of these genes were observed in spermatozoids. The addition of shikimic acid, a precursor of naphthoquinone pigments, to zygotes and embryos increased the expression of thepksandsultgenes. Our findings, including the development of specific conditions to promote pigment cell differentiation of embryonic sea urchin cells in culture, represent a definitive study on the molecular signaling pathways that are involved in the biosynthesis of pigments during sea urchin development.

Zygote ◽  
1999 ◽  
Vol 8 (S1) ◽  
pp. S42-S43 ◽  
Author(s):  
Tetsuya Kominami

Sea urchin pluteus larvae contain dozens of pigment cells in their ectoderm. These pigment cells are the descendants of the veg2 blastomeres of the 60-cell stage embryo. According to the fate map made by Ruffins and Ettensohn, the prospective pigment cells occupy the central region of the vegetal plate. Most of these prospective pigment cells exclusively give rise to pigment cells. Therefore, specification of the pigment cell lineage should occur at some point between the 60-cell and mesenchyme blastula stage. However, the detailed process of the specification of the pigment lineage is unknown.When are pigment cells specified? Are cell interactions necessary for the specification? Do founder cells exist? To answer these questions, I treated embryos with Ca2+-free seawater during the cleavage stage and examined the number of pigment cells observed in pluteus larvae. Treatment at 5.5–8.5 h and especially 7.5–10.5 h postfertilisation markedly reduced the number of pigment cells. The decrease was statistically significant. On the other hand, the treatment at 3.5–6.5 h or 9.5–12.5 h never reduced the number of pigment cells. By examining the frequency of the appearance of embryos whose numbers of pigment cells were less than 20, it was also found that the numbers of pigment cells were frequently in multiples of 4. Embryos having 4, 8, 12, 16 and 20 pigment cells were more frequently observed. Statistics indicated that the frequency of appearance was not random. These results indicated that cell contacts are necessary for the specification of pigment cells and that the specification occurs from 7 to 10 h postfertilisation. The results also suggest that the founder cells, if they exist, divide twice before they differentiate into pigment cells.


Development ◽  
1993 ◽  
Vol 117 (4) ◽  
pp. 1275-1285 ◽  
Author(s):  
C.A. Ettensohn ◽  
S.W. Ruffins

An interaction between the two principal populations of mesodermal cells in the sea urchin embryo, primary and secondary mesenchyme cells (PMCs and SMCs, respectively), regulates SMC fates and the process of skeletogenesis. In the undisturbed embryo, skeletal elements are produced exclusively by PMCs. Certain SMCs also have the ability to express a skeletogenic phenotype; however, signals transmitted by the PMCs direct these cells into alternative developmental pathways. In this study, a combination of fluorescent cell-labeling methods, embryo microsurgery and cell-specific molecular markers have been used to study the lineage, numbers, normal fate(s) and developmental potential of the skeletogenic SMCs. Previous fate-mapping studies have shown that SMCs are derived from the veg2 layer of blastomeres of the 64-cell-stage embryo and from the small micromeres. By specifically labeling the small micromeres with 5-bromodeoxyuridine, we demonstrate that descendants of these cells do not participate in skeletogenesis in PMC-depleted larvae, even though they are the closest lineal relatives of PMCs. Skeletogenic SMCs are therefore derived exclusively from the veg2 blastomeres. Because the SMCs are a heterogeneous population of cells, we have sought to gain information concerning the normal fate(s) of skeletogenic SMCs by determining whether specific cell types are reduced or absent in PMC(−) larvae. Of the four known SMC derivatives: pigment cells, blastocoelar (basal) cells, muscle cells and coelomic pouch cells, only pigment cells show a major reduction (> 50%) in number following SMC skeletogenesis. We therefore propose that the PMC-derived signal regulates a developmental switch, directing SMCs to adopt a pigment cell phenotype instead of a default (skeletogenic) fate. Ablation of SMCs at the late gastrula stage does not result in the recruitment of any additional skeletogenic cells, demonstrating that, by this stage, the number of SMCs with skeletogenic potential is restricted to 60–70 cells. Previous studies showed that during their switch to a skeletogenic fate, SMCs alter their migratory behavior and cell surface properties. In this study, we demonstrate that during conversion, SMCs become insensitive to the PMC-derived signal, while at the same time they acquire PMC-specific signaling properties.


Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1085-1091 ◽  
Author(s):  
R.A. Cameron ◽  
S.E. Fraser ◽  
R.J. Britten ◽  
E.H. Davidson

This paper examines the cell lineage relationships and cell fates in embryos of the sea urchin Strongylocentrotus purpuratus leading to the various cell types derived from the definitive vegetal plate territory or the veg2 tier of cells. These cell types are gut, pigment cells, basal cells and coelomic pouches. They are cell types that constitute embryonic structures through cellular migration or rearrangement unlike the relatively non-motile ectoderm cell types. For this analysis, we use previous knowledge of lineage to assign macromeres to one of four types: VOM, the oral macromere; VAM, the aboral macromere, right and left VLM, the lateral macromeres. Each of the four macromeres contributes progeny to all of the cell types that descend from the definitive vegetal plate. Thus in the gut each macromere contributes to the esophagus, stomach and intestine, and the stripe of labeled cells descendant from a macromere reflects the re-arrangement of cells that occurs during archenteron elongation. Pigment cell contributions exhibit no consistent pattern among the four macromeres, and are haphazardly distributed throughout the ectoderm. Gut and pigment cell contributions are thus radially symmetrical. In contrast, the VOM blastomere contributes to both of the coelomic pouches while the other three macromeres contribute to only one or the other pouch. The total of the macromere contribution amounts to 60% of the cells constituting the coelomic pouches.


Development ◽  
1979 ◽  
Vol 52 (1) ◽  
pp. 165-170
Author(s):  
Gillian J. MacMillan

The periodic albino mutant (apap) of Xenopus in which the development of melanophoresis impaired, is further reported here to possess an aberrant pattern of iridophore differentiation. The development of mutant and wild-type neural crest explants isolated in vesicles derived from tissues from identical and different genotypes was examined to determine if the mutant effect resides in the pigment cells or is mediated by the environmental tissues. Mutant melanophores and iridophores cultured in either mutant or wild-type tissues exhibited mutant patterns of differentiation. Wild-type pigment cells cultured in both wild-type and mutant tissues exhibited wild-type patterns of differentiation. Hence the mutation affects the capacities of melanoblasts and iridoblasts to differentiate but not the ability of the environmental tissues to support pigment cell differentiation.


Marine Drugs ◽  
2014 ◽  
Vol 12 (7) ◽  
pp. 3874-3891 ◽  
Author(s):  
Natalya Ageenko ◽  
Konstantin Kiselev ◽  
Pavel Dmitrenok ◽  
Nelly Odintsova

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hyo Sik Jang ◽  
Yujie Chen ◽  
Jiaxin Ge ◽  
Alicia N. Wilkening ◽  
Yiran Hou ◽  
...  

Abstract Background Zebrafish pigment cell differentiation provides an attractive model for studying cell fate progression as a neural crest progenitor engenders diverse cell types, including two morphologically distinct pigment cells: black melanophores and reflective iridophores. Nontrivial classical genetic and transcriptomic approaches have revealed essential molecular mechanisms and gene regulatory circuits that drive neural crest-derived cell fate decisions. However, how the epigenetic landscape contributes to pigment cell differentiation, especially in the context of iridophore cell fate, is poorly understood. Results We chart the global changes in the epigenetic landscape, including DNA methylation and chromatin accessibility, during neural crest differentiation into melanophores and iridophores to identify epigenetic determinants shaping cell type-specific gene expression. Motif enrichment in the epigenetically dynamic regions reveals putative transcription factors that might be responsible for driving pigment cell identity. Through this effort, in the relatively uncharacterized iridophores, we validate alx4a as a necessary and sufficient transcription factor for iridophore differentiation and present evidence on alx4a’s potential regulatory role in guanine synthesis pathway. Conclusions Pigment cell fate is marked by substantial DNA demethylation events coupled with dynamic chromatin accessibility to potentiate gene regulation through cis-regulatory control. Here, we provide a multi-omic resource for neural crest differentiation into melanophores and iridophores. This work led to the discovery and validation of iridophore-specific alx4a transcription factor.


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