Citation: Erkenbrack, E. M., Petsios, E. (2017). A conserved role for VEGF signaling in specification of homologous mesenchymal cell types positioned at spatially distinct developmental addresses in early development of sea urchins. J Exp Zool (Mol Dev Evol) 328(5): 423-432.
Divergence of ectodermal and mesodermal gene regulatory network linkages in early development of sea urchins
Developmental gene regulatory networks (GRNs) are assemblages of gene regulatory interactions that direct ontogeny of animal body plans. Studies of GRNs operating in the early development of euechinoid sea urchins have revealed that little appreciable change has occurred since their divergence ∼90 million years ago (mya). These observations suggest that strong conservation of GRN architecture was maintained in early development of the sea urchin lineage. Testing whether this holds for all sea urchins necessitates comparative analyses of echinoid taxa that diverged deeper in geological time. Recent studies highlighted extensive divergence of skeletogenic mesoderm specification in the sister clade of euechinoids, the cidaroids, suggesting that comparative analyses of cidaroid GRN architecture may confer a greater understanding of the evolutionary dynamics of developmental GRNs. Here I report spatiotemporal patterning of 55 regulatory genes and perturbation analyses of key regulatory genes involved in euechinoid oral–aboral patterning of nonskeletogenic mesodermal and ectodermal domains in early development of the cidaroid Eucidaris tribuloides. These results indicate that developmental GRNs directing mesodermal and ectodermal specification have undergone marked alterations since the divergence of cidaroids and euechinoids. Notably, statistical and clustering analyses of echinoid temporal gene expression datasets indicate that regulation of mesodermal genes has diverged more markedly than regulation of ectodermal genes. Although research on indirect-developing euechinoid sea urchins suggests strong conservation of GRN circuitry during early embryogenesis, this study indicates that since the divergence of cidaroids and euechinoids, developmental GRNs have undergone significant, cell type–biased alterations.
Placental invasion into the maternal endometrium of the uterus shows substantial similarities to early cancer dissemination into stroma1,2,3,4. These similarities have inspired the hypothesis of antagonistic pleiotropy5,6. According to this hypothesis, trophoblasts evolved the capacity to invade the endometrium, leading to invasive placentation. These mechanisms can become reactivated in cancer cells, leading to a predisposition to metastasis. This implies that cancer malignancy should be limited to placental mammals where invasive placentation first evolved. This prediction, however, is inconsistent with the fact that opossums, with ancestrally non-invasive placenta7,8, get invasive skin cancers9. Here, we explore an alternative scenario in which stromal cells of the uterus evolved to either resist or permit invasion, determining the outcome of placental invasiveness9.
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