The molecular mechanism underlying somite development differs along the embryonic antero-posterior axis. In zebrafish, cell lineage tracing and genetic analysis have revealed a difference in somite development between the trunk and tail. For instance, spadetail/tbx16 (spt) mutant embryos lack trunk somites but not tail ones. Trunk and tail somites are developed from mesodermal progenitor cells (MPCs) located in the tailbud. While the undifferentiated state of MPCs is maintained by mutual activation between Wnt and Brachyury/Ntl, the mechanism by which the MPCs differentiate into presomitic mesoderm (PSM) cells remains largely unclear. Especially, the molecules that promote PSM differentiation during tail development should be clarified. Here, we show that zebrafish embryos defective in mesogenin1 (msgn1) and spt failed to differentiate into PSM cells in tail development and show increased expression of wnt8 and ntl. Msgn1 acted in a cell-autonomous manner and as a transcriptional activator in PSM differentiation. The expression of msgn1 initially overlapped with that of ntl in the ventral tailbud, as previously reported; and its mis-expression caused ectopic expression of tbx24, a PSM marker gene, only in the tailbud and posterior notochord, both of which expressed ntl in zebrafish embryos. Furthermore, the PSM-inducing activity of misexpressed msgn1 was enhanced by co-expression with ntl. Thus, Msgn1 exercised its PSM-inducing activity in cells expressing ntl. Based on these results, we speculate that msgn1 expression in association with that of ntl may allow the differentiation of progenitor cells to proceed during development of somites in the tail.