Meeting Abstract
Chill susceptible insects, including the model species Drosophila melanogaster are incapacitated, injured, and killed by low temperature exposure before any freezing of their body fluids occurs, but adaptation and acclimation to low temperatures can facilitate substantial improvements in chilling tolerance. A growing body of recent studies on a range of insect models have suggested that injury and death at low temperatures are associated with a gradual loss of ion and water homeostasis across cellular membranes and epithelia. This loss of balance occurs most notably across the gut epithelia, where large ionic and osmotic gradients are constitutively maintained by high rates of transport. Dissipation of these gradients causes extracellular [K+] levels to increase, which causes cell depolarization and ultimately cell death at low temperatures. It remains unclear whether this cold-induced disruption of homeostasis is related to a greater net transcellular leak of ions and water through channels and aquaporins, respectively, or whether the occluding junctions between adjacent epithelial cells are disrupted by chilling. In this presentation, we will demonstrate that some of the major structural proteins of the septate junctions of Drosophila are differentially expressed during cold acclimation, and that these modifications are associated with a reduction in the tendency for paracellular solute leak across the midgut epithelium before and during chronic cold stress. Cold-acclimated flies also maintain low hemolymph [K+] during cold stress and consequently avoid chilling injury. Thus, specific changes to septate junction structure and stability likely aid in the maintenance of solute and water balance and may represent an important aspect of thermal acclimation with cascading metabolic and life history consequences.
