Induction of thermotolerance in T cells protects nuclear DNA topoisomerase I from heat stress.
In this study, we have demonstrated that topoisomerase I DNA relaxing activity is protected against a severe heat shock in T cells made thermotolerant by a prior modest heat treatment. However, following a severe heat-shock challenge and incubation at 37 degrees C, topoisomerase activity in the control population eventually returned to levels similar to those detected in thermotolerant cells. This recovery of topoisomerase activity appears to result from the renaturation of heat-inactivated enzyme rather than from synthesis of new protein because the rate of recovery of catalytic activity was not inhibited by the presence of the protein synthesis inhibitor, cycloheximide.
Ciavarra
R P
RP
Department of Microbiology, Eastern Virginia Medical School, Norfolk 23507-1696.
Duvall
W
W
Castora
F J
FJ
D000064:Acclimatization; D000818:Animals; D002467:Cell Nucleus / Q000201:enzymology*; D002478:Cells, Cultured; D003208:Concanavalin A; D003513:Cycloheximide / Q000494:pharmacology; D004261:DNA Replication; D004264:DNA Topoisomerases, Type I / Q000378:metabolism*; D006358:Hot Temperature; D007700:Kinetics; D008213:Lymphocyte Activation; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000201:enzymology* / Q000276:immunology; D013997:Time Factors
D003208:Concanavalin A; D003513:Cycloheximide; D004264:DNA Topoisomerases, Type I