These experiments address the mechanism of action of the persistence of proliferation in the cerebellar external granule layer (EGL) by comparing congenital hypothyroidism due to a recessive mutation in mice to thestaggerermouse mutant. In both cases persistence of the EGL can be demonstrated histologically, with the process more drawn out instaggererthan inhypothyroid.This correlates with higher than normal levels of the enzyme thymidine kinase, a biochemical marker of proliferation, in both mutants. It is hypothesized that the proliferation of EGL cells in both cases is controlled by effects of the mutations on the maturation rate of the Purkinje cells, possibly with other cell types as intermediates.