AbstractSomitogenesis is a fundamental segmentation process that forms the vertebrate body plan. A network of transcription factors is essential in establishing the spatial temporal order of this process. One such transcription factor is mesp-bawhich has an important role in determining somite boundary formation. Its expression in somitogenesis is tightly regulated by the transcriptional activator Tbx6 and the repressor Ripply1 via a feedback regulatory network. Loss offoxc1afunction in zebrafish leads to lack of anterior somite formation and reducedmesp-baexpression. Here we examine howfoxc1ainteracts with thetbx6-ripply1network to regulatemesp-baexpression. Infoxc1amorphants, anterior somites did not form at 12.5 hours post fertilization (hpf). At 22 hpf posterior somites formed, whereas anterior somites remained absent. Inripply1morphants, no somites were observed at any time point. The expression ofmesp-bawas reduced in thefoxc1amorphants and expanded anteriorly inripply1morphants. Thetbx6expression domain was smaller and shifted anteriorly in thefoxc1amorphants. Double knockdown offoxc1aandripply1resulted in absence of anterior somite formation while posterior somites did form, suggesting a partial rescue of theripply1phenotype. However, unlike the singlefoxc1amorphants, expression ofmesp-bawas restored in the anterior PSM. Expression oftbx6was expanded anteriorly in the double morphants. In conclusion, bothfoxc1aandripply1morphants displayed defects in somitogenesis, but their individual loss of function had opposing effects onmesp-baexpression. Loss ofripply1appears to have rescued themesp-ba expression in thefoxc1amorphant, suggesting that intersection of these parallel regulatory mechanisms is required for normalmesp-baexpression and somite formation.