SUMMARY: Lactose-limited chemostat populations of 418 showed hyper-β-galactosidase activity after 170 generations. Within the normally active phase, hyperactivity could be induced by adding thiomethyl-β--galactoside and was lost on its removal; natural hyper-activity was lost on transfer to a lactose medium in which ammonium was limiting. The ability of lactose to accelerate death from starvation was proportional to the β-galactosidase activity of the population. Cyclic AMP in the recovery medium alleviated lactose-accelerated death. Suppression of adenyl cyclase activity by traumatic substrates may be responsible for substrate-accelerated death.


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