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In studies of thermotolerance, large differences among higher taxa and small differences within a species are normally separate realms of investigation, with genetic experimentation currently feasible for only the latter. In the virilis group of Drosophila, however, species can be interbred to yield viable and partially fertile hybrids. Our research groups together have examined several species which replace one another along a latitutidinal gradient of temperature. The high-latitude species have lower thermotolerance. Hybrids are intermediate in thermotolerance. Reciprocal matings yield similar outcomes, consistent with an autosomal basis. Two species chosen for detailed study, D. virilis [low latitude] and D. lummei [high latitude], differ correspondingly in levels of heat-shock proteins. In situ hybridization to and the cloning and sequencing of the hsp68 and hsp70 genes reveal both inter-and intra-specific variation in hsp70 gene copy number due to both tandem duplication and pseudogenization. Extension of this analysis to multiple species pairs should permit a well-replicated analysis of the molecular basis of variation in thermotolerance among and within species. Supported by Russian Grants for Basic Science 0304-48-918 and 0204-49121, NSF grants IBN99-86158 and IBN03-16627.

Naturally-occurring heat shock (HS) during pupation induces abnormal wing development in Drosophila; we examined factors affecting the severity of this induction. The proportion of HS-surviving adults with abnormal wings varied with HS duration and intensity, and with the pupal age or stage at HS administration. Pretreatment (PT), mild hyperthermia delivered before HS, usually protected development against HS. Gradual heating resembling natural thermal regimes also protected wing development against thermal disruption. Because of the roles of the wings in flight and courtship and in view of natural thermal regimes that Drosophila undergo, both HS-induction of wing abnormalities and its abatement by PT may have marked effects on Drosophila in nature. Because PT is associated with expression of heat-inducible molecular chaperones such as Hsp70 in Drosophila, we compared thermal disruption of wing development among hsp70 mutants as well as among strains naturally varying in Hsp70 levels. Contrary to expectations, lines or strains with increased Hsp70 levels were no more resistant to HS-disruption of wing development than counterparts with lower Hsp70 levels. In fact, wing development was more resistant to HS in hsp70 deletion strains than control strains. We suggest that, while high Hsp70 levels may aid cells in surviving hyperthermia, high levels may also overly stimulate or inhibit numerous signaling pathways involved in cell proliferation, maturation, and programmed death, resulting in developmental failure.