Abstract
Heat shock proteins (Hsps) act as molecular chaperones involved in protein folding/refolding and the prevention of toxic proteins aggregation. Ubiquitous and targeted expressions of certain heat shock proteins have been reported to extend lifespan and increase resistance to environmental stresses in Drosophila. Here, we report that the neuronal expression of UAS-hsp26 by elav-GAL4 displays a longer lifespan and an increased oxidative resistance in Drosophila melanogaster. In contrast to the effects of hsp27, the neuronal expression of UAS-hsp26 does not rescue the polyglutamine (41Q)-induced toxicity, paraquat elicited Parkinsonism like disorder, and the lethality by apoptosis inducing genes in Drosophila. It suggests that there are some differential functions between hsp26 and hsp27. A detailed study to identify the sub-regions of neurons responsible for the lifespan extension by the expression of UAS-hsp26 reveals that the whole brain region GAL4 driver or the antennal and optic lobe GAL4 driver are able to enhance lifespan and oxidative stress resistance upon the hsp26 expression, but not be able by some other drivers. Together, the neuronal expression of UAS-hsp26 exhibits increased lifespan and stress resistance, but not on the prevention of the neurodegeneration and apoptosis in Drosophila.