ECB-ART-41263Evol Dev 2009 Jan 01;115:560-73. doi: 10.1111/j.1525-142X.2009.00362.x.
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An evolutionary transition of Vasa regulation in echinoderms.
Vasa, a DEAD box helicase, is a germline marker that may also function in multipotent cells. In the embryo of the sea urchin Strongylocentrotus purpuratus, Vasa protein is posttranscriptionally enriched in the small micromere lineage, which results from two asymmetric cleavage divisions early in development. The cells of this lineage are subsequently set aside during embryogenesis for use in constructing the adult rudiment. Although this mode of indirect development is prevalent among echinoderms, early asymmetric cleavage divisions are a derived feature in this phylum. The goal of this study is to explore how vasa is regulated in key members of the phylum with respect to the evolution of the micromere and small micromere lineages. We find that although striking similarities exist between the vasa mRNA expression patterns of several sea urchins and sea stars, the time frame of enriched protein expression differs significantly. These results suggest that a conserved mechanism of vasa regulation was shifted earlier in sea urchin embryogenesis with the derivation of micromeres. These data also shed light on the phenotype of a sea urchin embryo upon removal of the Vasa-positive micromeres, which appears to revert to a basal mechanism used by extant sea stars and pencil urchins to regulate Vasa protein accumulation. Furthermore, in all echinoderms tested here, Vasa protein and/or message is enriched in the larval coelomic pouches, the site of adult rudiment formation, thus suggesting a conserved role for vasa in undifferentiated multipotent cells set aside during embryogenesis for use in juvenile development.
PubMed ID: 19754712
PMC ID: PMC3034130
Article link: Evol Dev
Genes referenced: ddx4 LOC100887844 LOC105441782 LOC583082 LOC587482
Antibodies: ddx4 Ab1 ddx4 Ab2
References [+] :
Altschul, Gapped BLAST and PSI-BLAST: a new generation of protein database search programs. 1997, Pubmed