Faivre-Sarrailh C, Rabié A
C.N.R.S. UA 1197, Université des Sciences et Techniques du Languedoc, Montpellier, France.
Brain Res. 1988 Jun 1;469(1-2):293-7. doi: 10.1016/0165-3806(88)90190-3.
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.
利用脱氧核糖核酸酶I抑制试验,在存在或不存在盐酸胍(其使肌动蛋白丝解聚)的情况下,测定正常和甲状腺功能减退大鼠小脑内总肌动蛋白和丝状肌动蛋白的发育变化。甲状腺功能减退并未改变每毫克蛋白质中总肌动蛋白的含量。与正常动物一样,它在8日龄左右达到最大值,然后下降直至成年。相比之下,丝状肌动蛋白的比例在正常发育过程中于出生后第一周后增加,但在甲状腺功能缺乏的大鼠中显著降低,仅在35日龄时达到正常值。甲状腺素治疗至少4天可使丝状肌动蛋白含量在14天时恢复正常。本研究表明,甲状腺激素的形态发生作用不仅如先前所述作用于微管装置,还部分通过控制肌动蛋白单体 - 聚合物平衡来发挥作用。