When pluteus embryos of Lytechinus pictus were treated with colcemid, the incorporation of [35S]meth- ionine into tubulin declined by 5- to 15-fold within 4 h. This was mostly accounted for by a rapid decline in the concentration of α- and β-tubulin mRNA in the cytoplasm. Treatment with other microtubule depoly- merizing agents (colchicine, nocodazole, low concen- trations of vinblastine) had similar effects. Treatment of embryos with the microtubule-stabilizing agent, taxol, or high concentrations of vinblastine resulted in increased synthesis of tubulin. The concentration of tubulin mRNA increases during development and becomes increasingly sensitive to colcemid and de- creasingly sensitive to taxol. The transcriptional ac- tivity of tubulin genes, estimated by an RNA run-on assay in isolated nuclei, was not altered after colcemid treatment. On the other hand, the rate of decay of tubulin mRNA in prism embryos treated with actino- mycin D was increased several fold by colcemid treatment, while taxol treatment led to an increased half-life of tubulin mRNA. These observations suggest that tubulin synthesis is autogenously regulated at the level of mRNA stability by the level of unpolymerized tubulin. The increasing polymerization of micro- tubules and declining level of unpolymerized tubulin during embryogenesis would result in a stabilization of tubulin mRNA accounting for the increasing concen- tration of tubulin mRNA and rate of tubulin synthesis, as well as the increasing sensitivity of tubulin synthesis to microtubule-depolymerizing agents. Evidence is also presented for a rapid influence of the level of unpolymerized tubulin on the efficiency of translation of tubulin mRNA.

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