secretion by temperature cycling was a transient phenomenon, and recovery required new protein synthesis. As the micronemes in these treated cells are not empty of their contents, but simply refractory to secretion, we speculate that the defect may lie in the discharge event. One possibility is that a labile factor in the secretion apparatus is exhausted during the initial discharge, and this component must be resynthesized before subsequent discharges can occur. Thistransitory response isconsistentwithour observations of microneme secretion during host cell invasion, which indicate that the initial rapid discharge is followed by a shut-off in further secretion as the parasite enters the host cell.