Induction of the heat shock regulon does not produce thermotolerance in Escherichia coli.

The addition of isopropyl thio-beta-D-galactoside (IPTG) to Escherichia coli cells containing multiple copies of the heat shock regulatory gene htpR (rpoH) under the control of an IPTG-inducible promoter (P-tac) induced 15 of the 17 polypeptides of the heat shock (HTP) regulon. The time course and magnitude of the induction closely resembled that caused by a shift to 42 degrees C. Nevertheless the two means of inducing the heat shock regulon differed in outcome. Cultures grown at 28 degrees C and induced by incubation at 42 degrees C for 15 min gave significant protection against a challenge temperature of 50 degrees C, but no protection was afforded by a 15-min IPTG treatment at 28 degrees C. It could be shown that there was no interference by IPTG with the development of thermotolerance at 42 degrees C. Also, treatment of a wild strain of E. coli with various toxic agents revealed no correlation between the development of thermotolerance and the induction of any subset of the heat shock proteins. Thermotolerance appears to develop by processes other than the htpR-dependent induction of heat shock proteins.

Triacylglycerol contents and in vivo lipogenesis of ob/ob, db/db and Avy/a mice.

The triacylglycerol content and the in vivo lipogenesis rates of the liver and the carcass of 12 groups of mice were studied. They were mice of three strains and affected by mutations at three loci: C57BL/6J-ob/ob and normal mice; C57BL/KsJ-db/db and normal mice; and VY/WfL-Avy/a and normal mice. Each type of mice was studied at two body weight levels, before and after the mutants became grossly obese. It was found that the C57BL/6J-ob/ob and the C57BL/KsJ-db/db mice had the characteristics of juvenile type obesity. They had higher lipogenesis rates and accumulated more triacylglycerol when they were young. They gained weight rapidly mainly due to the accumulation of more triacylglycerol as they matured. Their total triacylglycerol content could reach 50% of their body weight. At maturity, their lipogenesis rates had decreased to normal. In contrast, the VY/WfL-Avy/a mice had the characteristics of maturity-onset type obesity. When they were young, they did not have higher lipogenesis rates and had only a moderate amount of triacylglycerol stored. They did not gain weight rapidly as they matured. However, when they reached maturity, their lipogenesis rate did not decrease. Their body triacylglycerol content was about 25% of their weight.