For proper animal development, tissues and organs require sufficient oxygen; defects in oxygen supply (hypoxia) can cause developmental disorders(1). In humans, disrupted oxygen supply underlies many diseases(2). Although tissue-culture studies have revealed much about adaptation to hypoxia at the cellular level(3 4), less is known of what mediates whole-body responses. My research employs Drosophila to study how hypoxia affects development at the organismal level. Drosophila larvae have evolved to grow on decaying food – an environment of low ambient oxygen(5–8). Hence, they provide a good genetic model to study how hypoxia influences physiology and development. In the lab, larvae exposed to hypoxia (5% O2) adapt by reducing their growth and delaying development to the pupal stage. However, the molecular bases for these adaptations remain unclear. The larval-pupal developmental transition is controlled by a neuroendocrine pathway involving the prothoracic gland (PG), an endocrine organ that produces the maturation steroid hormone ecdysone (9,10). At the end of the larval period, neuronal input to the PG triggers autocrine signaling through the conserved Epidermal Growth Factor Receptor (Egfr)/MAP kinase (ERK) pathway, which induces the PG to synthesize and release ecdysone(11). This ecdysone acts on all tissues to initiate maturation(11). My data suggest this autocrine Egf/ERK signaling is blunted in hypoxia, thus delaying the developmental transition. Since signaling and key aspects of steroid hormone regulation are conserved between Drosophila and humans (9,10,12), my work provides insights into how the program of development can adapt to fluctuating environmental conditions.