Cooperative function of deltaC and her7 in anterior segment formation

A combined loss of the cyclic Her genes her1 and her7 disrupts segmentation of both anterior and posterior paraxial mesoderm, indicating that her genes function redundantly in anterior segmentation. To test whether this anterior redundancy is specific to the her gene family, or alternatively is a more global feature of the segmentation oscillator, we looked at anterior segmentation after morpholino knock down of the cyclic cell-surface Notch ligand deltaC (dlc), either alone or in combination with her7, or other Delta/Notch pathway genes. We find that dlc is required for coherence of wavelike expression domains of cyclic genes her1 and her7 and maintenance of their expression levels, as well as for cyclic transcription of dlc itself, confirming that dlc is a component of the segmentation oscillator. Dose dependent, posteriorly-restricted segmentation defects were seen in the dlc knock down, and in combination with the deltaD or notch1a mutants. However, combined reduction of function of dlc and her7 results in defective segmentation of both anterior and posterior paraxial mesoderm, and a failure of cyclic expression domains to initiate, similar to loss of both her genes. Thus, anterior segmentation requires the functions of both her and delta family members in a parallel manner, suggesting that the segmentation oscillator operates in paraxial mesoderm along the entire vertebrate axis.