Abstract

Using a DNase I inhibition assay, in the presence or the absence of guanidine hydrochloride (which depolymerizes the actin filaments), developmental changes in total and filamentous actin were determined in the cerebellum of normal and hypothyroid rats. The total actin content per mg protein was not modified by hypothyroidism. As in normal animals, it reached a maximum around the age of 8 days and then decreased until adulthood. In contrast, the proportion of filamentous actin, which increased after the first postnatal week during normal development, was significantly reduced in the thyroid-deficient rats, only reaching normal values at 35 days. Thyroxine treatment for at least 4 days returned the filamentous actin content to normal at 14 days. The present study shows that the morphogenetic action of thyroid hormone is exerted not only on the microtubular apparatus, as previously described, but also in part through a control of actin monomer-polymer equilibrium.

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