Adaxial cell migration in the zebrafish embryo is an active cell autonomous property that requires the Prdm1a transcription factor

• Adaxial cells migrate cell-autonomously during zebrafish somitogenesis.
• Adaxial cells become polarised and extend filopodia at their leading edge.
• Prdm1a controls adaxial cell migration independently of Sox6 function.
• M- and N-cadherin expression in myotome is largely independent of Prdm1a function.

Adaxial cells, the progenitors of slow-twitch muscle fibres in zebrafish, exhibit a stereotypic migratory behaviour during somitogenesis. Although this process is known to be disrupted in various mutants, its precise nature has remained unclear. Here, using in vivo imaging and chimera analysis, we show that adaxial cell migration is a cell autonomous process, during which cells become polarised and extend filopodia at their leading edge. Loss of function of the Prdm1a transcription factor disrupts the polarisation and migration of adaxial cells, reflecting a role that is independent of its repression of sox6 expression. Expression of the M- and N-cadherins, previously implicated in driving adaxial cell migration, is largely unaffected by loss of Prdm1a function, suggesting that differential cadherin expression is not sufficient for adaxial cell migration.