An Ets transcription factor, HrEts, is target of FGF signaling and involved in induction of notochord, mesenchyme, and brain in ascidian embryos

AbstractIn ascidian embryos, a fibroblast growth factor (FGF) signal induces notochord, mesenchyme, and brain formation. Although a conserved Ras/MAPK pathway is known to be involved in this signaling, the target transcription factor of this signaling cascade has remained unknown. We have isolated HrEts, an ascidian homolog of vertebrate Ets1 and Ets2, to elucidate the transcription factor involved in the FGF signaling pathway in embryos of the ascidian Halocynthia roretzi. Maternal mRNA of HrEts was detected throughout the entire egg cytoplasm and early embryos. Its zygotic expression started in several tissues, including the notochord and neural plate. Overexpression of HrEts mRNA did not affect the general organization of the tadpoles, but resulted in formation of excess sensory pigment cells. In contrast, suppression of HrEts function by morpholino antisense oligonucleotide resulted in severe abnormalities, similar to those of embryos in which the FGF signaling pathway was inhibited. Notochord-specific Brachyury expression at cleavage stage and notochord differentiation at the tailbud stage were abrogated. Formation of mesenchyme cells was also suppressed, and the mesenchyme precursors assumed muscle fate. In addition, expression of Otx in brain-lineage blastomeres was specifically suppressed. These results suggest that an Ets transcription factor, HrEts, is involved in signal transduction of FGF commonly in notochord, mesenchyme, and brain induction in ascidian embryos