Meeting Abstract
Chill susceptible insects, like the migratory locust, often die due to an accumulation of injuries unrelated to freezing when exposed to low temperatures. These injuries, known as chilling injuries, are consistently associated with ion imbalance across the gut epithelia. It has been recently suggested that this imbalance is at least partly driven by cold-induced disruption of epithelial barrier function. Here, we aim to test this hypothesis in the migratory locust. To quantify chill tolerance, locusts were exposed to -2˚C for various durations and monitors for chill coma recovery time and survival 24h post-cold exposure. Longer exposure times significantly increased recovery time and caused injury and death. Barrier failure was tested by monitoring movement of an epithelial barrier marker (FITC-dextran) across the gut epithelia during exposure to -2˚C. There was minimal marker movement across the epithelia in the cold, suggesting that locust gut barrier function is generally conserved during chilling. We then monitored ion movement during cold exposure. Contrary to previous results, cold-induced ion imbalance still occurred. This finding may be a consequence of the large, polar, and uncharged nature of FITC-dextran, and small ions may yet leak in the cold. A similar approach was therefore undertaken to investigate gut permeability, this time using the smaller fluorescently-labelled PEG as our marker to determine if size was in fact the limiting factor in our results.
