Hypoxia-induced gene expression changes in N. vectensis embryos

O2 availability is one of the critical drivers of metazoan evolution and diversification. The earliest metazoans evolved in shallow marine shelves of the Neoproterozoic era, where the redox environment was likely variable and spatially heterogenous. This imposed physiological constraints on the emerging animals, selecting for O2-responsive and stress-adaptive traits. Embryogenesis is a novel and highly conserved stage of metazoan development, and its regulatory architecture may hold the key to understanding how adaptive traits arise in response to environmental change. Defining how early metazoan embryos respond to fluctuating O2 levels will therefore provide essential insights into the adaptive mechanisms that shaped the evolution of metazoans. Here, the embryos of the cnidarian Nematostella vectensis, a representative of early-diverging metazoans, were used to comprehensively investigate the developmental and genetic responses to hypoxia. N. vectensis embryogenesis is O2-dependent, with hypoxia inducing a reversible developmental arrest. Transcriptomic profiling reveals that the hypoxia response in N. vectensis embryos is conserved with bilaterians, encompassing core hypoxia-responsive genes and pathways. These findings suggest that the genetic toolkit underlying embryonic hypoxia responses was already established in the common cnidarian–bilaterian ancestor.