Functional characteristics of untranslated messenger ribonucleoprotein particles from mouse sarcoma ascites cells. Possible relation to the control of messenger RNA utilization

BERGMANN, I.E; CEREGHINI, S.; GEOGHEGAN, T.; BRAWERMAN, G.

JOURNAL OF MOLECULAR BIOLOGY

Año: 1982 vol. 156 p. 567 - 582

0022-2836

A portion of the messenger RNA of mouse sarcoma ascites cells occurs as untranslated nucleoprotein particles. These sediment as discrete entities, apparently not attached to other cytoplasmic structures. The RNP§ particles are translated very poorly in the reticulocyte cell-free system, but yield active mRNA upon deproteinization. In contrast, mRNPs generated by runoff from polysomes in starved cells tend to be about as active as the free RNA. The mRNA in the untranslated mRNPs appears to be masked by protein components that prevent its interaction with the protein-synthesizing machinery. The low activity of these mRNPs in the cell-free system cannot be attributed to the presence in the preparations of non-specific inhibitors of translation, as indicated by the fact that they cause little or no inhibition of translation of the active runoff mRNPs in mixed incubations. Exposure of the mRNPs to 0.5 to 0.8 -NaCl causes varying degrees of activation of individual mRNA species. A portion of the untranslated mRNPs are driven into polysomes when the ascites cells are exposed briefly to low levels of cycloheximide. The species susceptible to this apparent activation show the same characteristics in vitro as those that remain untranslated in the drug-treated cells. They are equally ineffective as RNPs in the reticulocyte cell-free system, and they exhibit similar susceptibilities to activation by salt. We suggest that the maintenance of these RNA molecules in an inactive state in the cell serves to regulate the rate of synthesis of the corresponding polypeptides. Such a regulation could be achieved through polypeptides capable of preventing the translation of their own mRNAs. Excessive production of such polypeptides would then result in feedback inhibition of their synthesis.