Maternal and zygotic ß-catenin function in the sea anemone

A vast majority of animals belong to a group called Bilateria, the members of which are characterized by possessing two body axes the posterior-anterior and the dorsal-ventral. In bilaterian embryos, beta-catenin signalling is critical for two consecutive processes occurring very early during development. First, maternally deposited beta-catenin specifies the endomesoderm, an embryonic region which will split into two germ layers called endoderm and mesoderm. Together, they will give rise to the inner organs of the animal. Second, Wnt signalling activates zygotically produced beta- catenin, which patterns the posterior-anterior body axis. The mechanism of Wnt/beta-catenin- dependent axis patterning is older than Bilateria it is shared between Bilateria and their evolutionary sister group Cnidaria (sea anemones, corals, jellyfish) indicating that it has be inherited by both these groups from their common ancestor some 650-700 million years ago. Evolutionary conservation was also suggested for the beta-catenin-dependent mechanism of endomesoderm specification, however, recently we showed that in the sea anemone Nematostella this is not the case. There, instead of specifying endomesoderm, maternal beta-catenin specified everything except endomesoderm and prevented endomesoderm specification in the wrong place. The main goal of the new FWF-funded project is to understand this strange regulatory behaviour and find out why beta-catenin does not accumulate in the future endomesodermal cells, what specifies the endomesoderm if it is not the maternal beta-catenin, and how beta-catenin accumulation prevents endomesoderm specification in the non-endomesodermal cells. This analysis will allow us to better understand the evolution of animal germ layers and patterning mechanisms. The second part of the project will be devoted to investigating the mechanism of posterior-anterior patterning of the mesoderm in Nematostella and the role of Wnt/beta-catenin in it. As mentioned above, endomesoderm forms in the beta-catenin-negative domain of the embryo and then segregates into endoderm, which becomes beta-catenin-positive, and mesoderm, which remains beta-catenin negative until larval stages. However, later in development, Wnt genes start to be expressed in staggered domains in the mesoderm as it starts to become patterned along the posterior-anterior axis. Currently, nothing is known about how mesodermal patterning is regulated, however, we expect involvement of the Wnt/beta-catenin signaling. In this project, we will systematically address the function of mesodermal Wnt genes and identify direct transcriptional targets of Wnt/beta-catenin signalling to reveal the patterning logic subdividing the mesoderm of our model into distinct spatial domains.