Somitogenesis 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-ba which 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 of foxc1a function in zebrafish leads to lack of anterior somite formation and reduced mesp-ba expression. Here we examine how foxc1a interacts with the tbx6-ripply1 network to regulate mesp-ba expression. In foxc1a morphants, anterior somites did not form at 12.5 hours post fertilization (hpf). At 22 hpf posterior somites formed, whereas anterior somites remained absent. In ripply1 morphants, no somites were observed at any time point. The expression of mesp-ba was reduced in the foxc1a morphants and expanded anteriorly in ripply1 morphants. The tbx6 expression domain was smaller and shifted anteriorly in the foxc1a morphants. Double knockdown of foxc1a and ripply1 resulted in absence of anterior somite formation while posterior somites did form, suggesting a partial rescue of the ripply1 phenotype. However, unlike the single foxc1a morphants, expression of mesp-ba was restored in the anterior PSM. Expression of tbx6 was expanded anteriorly in the double morphants. In conclusion, both foxc1a and ripply1 morphants displayed defects in somitogenesis, but their individual loss of function had opposing effects on mesp-ba expression. Loss of ripply1 appears to have rescued the mesp-ba expression in the foxc1a morphant, suggesting that intersection of these parallel regulatory mechanisms is required for normal mesp-ba expression and somite formation.
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