Meeting Abstract
Global warming is driving species beyond their thermal physiological limit. Oviparous species, such as reptiles, may be negatively impacted by climate change as their eggs will be laid and incubated at progressively higher temperatures. Anolis lizards subjected to thermal stress during early embryonic development experience decreased survival and increased rates of craniofacial malformation, yet the mechanisms driving these patterns remain unknown. It has been suggested that oxygen restriction sets the thermal range of embryonic development (i.e., oxygen limitation hypothesis). We hypothesized that hypoxic conditions would lower the thermal threshold of Anolis embryos while hyperoxic conditions would buffer the effects of thermal stress. We discovered that embryos developing under hypoxia at sublethal temperatures produced craniofacial malformations similar to thermally stressed anole embryos. In contrast, embryos developing under hyperoxic conditions and typically lethal temperatures developed normally. To clarify the potential role of oxidative stress, we measured the activity of the antioxidant enzyme superoxide dismutase (SOD) in anole embryos incubated at varying temperatures. Initial trials show that increased temperature leads to increased SOD activity in the developing head and brain. Additionally, preliminary results indicate a hypoxia marker, Hypoxia inducible factor 1-alpha, is present in the developing brain of thermally stressed anole embryos. Our results suggest that oxygen limitation and oxidative stress may explain how structural malformations arise during embryonic thermal stress, and why survival is negatively impacted at high temperatures. We elucidate a potential mechanism of induced craniofacial defects in thermally stressed lizard embryos.
