Asymmetric cell divisions play crucial roles during ascidian embryogenesis. In these processes, an FGF signaling is an essential inductive signal for establishing cell fate polarization, such as mesenchyme and notochord. It was well reported that the FGF signaling cascade is composed of FGF, FGF receptor, Ras, MEK, Erk and Ets. However, mechanisms of communication between the FGF and other signaling pathways and of integrated regulation of signaling pathways have remained largely unknown. In this study, we isolated HrS6K, a homologue of the S6K gene that belongs to the S6-H1 kinase of the ribosomal S6 kinase family, and HrNck1, a homologue of Nck1 gene that encodes an adaptor protein containing Src homology 2 and 3 domains, from the ascidian Halocynthia roretzi, to elucidate the mechanisms. Zygotic expression of HrS6K was initiated as early as the 16-cell stage. In the 64-cell stage embryos, expression of HrS6K was seen in mesenchyme precursor cells. The signal was detected in dorsal midline cells and mesenchyme clusters of the early tailbud embryos, and then down-regulated by the late tailbud stage. In adults, HrS6K mRNA was highly detected in muscle and stomach by QPCR method. On the other hand, HrNck1 transcripts are detected maternally. Zygotic HrNck1 mRNA was strongly expressed in mesenchyme clusters of the neurula, and in tail tip cells of the early tailbud embryos. These results suggest that HrS6K and HrNck1 are involved in formation of mesenchyme cells, which are specified by the FGF signaling.