her1 and her13.2 are jointly required for somitic border specification along 
the entire axis of the fish embryo

Sieger, D.; Ackermann, B.; Winkler, C.; Tautz, D.; Gajewski, M.

doi:10.1016/j.ydbio.2006.02.003

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her1 and her13.2 are jointly required for somitic border specification along the entire axis of the fish embryo

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Sieger, D., Ackermann, B., Winkler, C., Tautz, D., & Gajewski, M. (2006). her1 and her13.2 are jointly required for somitic border specification along the entire axis of the fish embryo. Developmental Biology, 293(1), 242-251. doi:10.1016/j.ydbio.2006.02.003.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-0E2A-8

Abstract

Delta-Notch and FGF signaling are involved in the control of somitogenesis in zebrafish. her genes are generally known as downstream targets of Delta-Notch signaling, but the her13.2 gene from zebrafish has recently been shown to depend on FGF signaling only. We have here studied the functional role of her13.2 in conjunction with her genes that are under Delta-Notch control. We show that joint inactivation of her1 and her13.2 leads to a complete loss of all somitic borders, including the most anterior ones. This somitic phenotype is much stronger than would be expected from the effects of the inactivation of either gene alone. A joint inactivation of her13.2 and her7, which is a paralogue of her1, does not show this enhanced effect. Thus, our results confirm inferences from in vitro studies that her1 and her13.2 form specific heterodimers, which may directly be required for regulating further target genes. These two her genes thus constitute the link between Delta-Notch pathway and FGF signaling during entire somitogenesis. We show that this interaction is conserved in the rice fish medaka, as a joint inactivation of the respective orthologues leads also to the same phenotype as in zebrafish. In addition, our results suggest that the mechanisms for anterior and posterior somite formation are not principally different, although the anterior somites often seem more refractory to genetic perturbations. (c) 2006 Elsevier Inc. All rights reserved.