Walker P R, Whitfield J F
J Biol Chem. 1985 Jan 25;260(2):765-70.
Colchicine, at low intracellular concentrations, causes a rapid depolymerization of membrane-associated polyribosomes. Poly(A+) mRNA is rapidly lost from these polysomes, and 80 S monomers are left attached to the membranes of the endoplasmic reticulum. Binding studies and measurements of intracellular colchicine concentrations indicate that the drug is acting via depolymerization of cytoplasmic microtubules. The vinca alkaloids, vincristine and vinblastine, have the same effect on polyribosomes, whereas lumicolchicine is ineffective. Furthermore, cordycepin and actinomycin D are without effect on polyribosomes indicating that colchicine is not simply inhibiting the production or transport of new mRNA. It appears that disruption of the cytoplasmic microtubule network prevents membrane-associated ribosomes from reinitiating protein synthesis resulting in the rapid loss of mRNA.
秋水仙碱在低细胞内浓度时,会导致膜相关多核糖体迅速解聚。多聚腺苷酸(Poly(A+))mRNA会迅速从这些多核糖体上丢失,而80S单体则留在内质网的膜上。结合研究和细胞内秋水仙碱浓度的测量表明,该药物是通过细胞质微管的解聚起作用的。长春花生物碱长春新碱和长春碱对多核糖体有相同的作用,而光秋水仙碱则无效。此外,虫草素和放线菌素D对多核糖体没有影响,这表明秋水仙碱并非简单地抑制新mRNA的产生或运输。看来细胞质微管网络的破坏会阻止膜相关核糖体重新启动蛋白质合成,从而导致mRNA迅速丢失。