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Animal embryos and human fetus respond to hypoxia(reduced oxygen availability)by slowing down or arresting their developmental processes.Upon re-oxygenation,they show compensatory acceleration in developmental rate.Likewise,starvation or undernourishment reduces growth rate in young animals ranging from insects to humans.This plasticity,referred as developmental plasticity,is not only found in the animal kingdom but also in bacteria and fungi(i.e.spore formation)as well as plants(i.e.seed dormancy).Although developmental and phenotypic plasticity is found in all major domains of life and is considered a key driving force in the evolution of structural and physiological innovations,we have a limited understanding of the underlying mechanisms.A mechanistic understanding of developmental plasticity also has important biomedical implications because impaired plasticity often leads to diseases.The human endocrine pancreas,for instance,shows increased β cell mass when facing increased insulin demands,such as insulin insensitivity.Impaired pancreas plasticity results in a decrease in functional β cell mass,which will lead to impaired glucose homeostasis and the development of type II diabetes.Recent studies in zebrafish suggest that changes in many environmental cues influence growth and development through the insulin/insulin-like growth factor(IIS)signaling systems.In this talk,I will present recent findings using the zebrafish model on how hypoxia,nutrient deficiency,and acidic environment influence the growth and developmental processes by altering key players in the IIS signaling pathway.