SoxE genes are multifunctional transcriptional regulators that play key roles in specification and differentiation of neural crest. Three members (Sox8, Sox9, Sox10) are expressed in the neural crest and are thought to modulate the expression and activity of each other. In addition to regulating the expression of other early neural crest marker genes, SoxE genes are required for development of cartilage. Here we investigated the role of SoxE genes in development of the neural crest-derived branchial skeleton in the sea lamprey. Using a morpholino knockdown approach, we show that all three SoxE genes described in lamprey are required for branchial basket development. Our results suggest that SoxE1 and SoxE2 are required for specification of the chondrogenic neural crest. SoxE3 plays a morphogenetic role in patterning of the branchial basket and may be required for the development of mucocartilage, a tissue unique to larval lampreys. While the lamprey branchial basket develops primarily from an elastin-like major extracellular matrix protein that is specific to lampreys, fibrillar collagen is also expressed in developing branchial cartilage and may be regulated by the lamprey SoxE genes. Our data suggest that the regulation of Type II collagen by Sox9 might have been co-opted by the neural crest in development of the branchial skeleton following the divergence of agnathan and gnathostome vertebrates. Finally, our results also have implications for understanding the independent evolution of duplicated SoxE genes among agnathan and gnathostome vertebrates.
The members of the AP-2 family of transcription factors play important roles during mammalian development and morphogenesis. AP-2γ (Tcfap2c – Mouse Genome Informatics) is a retinoic acid-responsive gene implicated in placental development and the progression of human breast cancer. We show that AP-2γ is present in all cells of preimplantation embryos and becomes restricted to the extra-embryonic lineages at the time of implantation. To study further the biological function of AP-2γ, we have generated Tcfap2c-deficient mice by gene disruption. The majority of Tcfap2c–/– mice failed to survive beyond 8.5 days post coitum (d.p.c.). At 7.5 d.p.c., Tcfap2c–/– mutants were typically arrested or retarded in their embryonic development in comparison to controls. Morphological and molecular analyses of mutants revealed that gastrulation could be initiated and that anterior-posterior patterning of the epiblast remained intact. However, the Tcfap2c mutants failed to establish a normal maternal-embryonic interface, and the extra-embryonic tissues were malformed. Moreover, the trophoblast-specific expression of eomesodermin and Cdx2, two genes implicated in FGF-responsive trophoblast stem cell maintenance, was significantly reduced. Chimera studies demonstrated that AP-2γ plays no major autonomous role in the development of the embryo proper. By contrast, the presence of AP-2γ in the extra-embryonic membranes is required for normal development of this compartment and also for survival of the mouse embryo.
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