THE three known and well characterized amber suppressors1 are almost certainly transfer RNAs altered by single base substitutions in their anticodons, the altered anticodon being the complement to the amber codon (UAG)1–6. Studies on the conversion of these amber suppressors to ochre suppressors, presumed still to be charged with the same amino-acids, showed that at least these three ochre suppressors are probably also transfer RNAs with altered anticodons5,6. As a result of previous work, we had at our disposal cells containing no suppressor (su−), a class 1 amber suppressor presumed to insert serine, and a class 1 ochre suppressor also presumed to insert serine. Cells containing a class 1 amber suppressor were derived from an su− parent cell, probably by a single base change in the DNA information specifying the anticodon of a seryl-transfer RNA. Cells containing a class 1 ochre suppressor were derived from cells containing a class 1 amber suppressor by suppressor conversion5. The growth characteristics of su− cells and cells containing a class 1 amber suppressor are always similar, and differ from those for cells containing a class 1 ochre suppressor. The latter cells usually have reduced growth rates, support the growth of a smaller number of amber mutants of T4 phage, and give rise to reduced burst sizes of T4+. These effects of the presence of an ochre suppressor could result from anticodon–codon (UUA–UAA) interactions if UAA codons are normally used as chain terminators during translation.
Subscribe to Journal
Get full journal access for 1 year
only $3.83 per issue
All prices are NET prices.
VAT will be added later in the checkout.
Rent or Buy article
Get time limited or full article access on ReadCube.
All prices are NET prices.
Garen, A., Science, 160, 149 (1968).
Landy, A., Abelson, J., Goodman, H. M., and Smith, J. D., J. Mol. Biol., 29, 457 (1967).
Goodman, H. M., Abelson, J., Landy, A., Brenner, S., and Smith, J. D., Nature, 217, 1019 (1968).
Andoh, T., and Ozeki, H., Proc. US Nat. Acad. Sci., 59, 792 (1968).
Person, S., and Osborn, M., Proc. US Nat. Acad. Sci., 60, 1030 (1968).
Ohlsson, B. M., Strigini, P. F., and Beckwith, J. R., J. Mol. Biol., 36, 209 (1968).
Osborn, M., and Person, S., Mutation Res., 4, 504 (1967).
Person, S., and Bockrath, R. C., Biophys. J., 4, 355 (1964).
Revel, H. R., Luria, S. E., and Rotman, B., Proc. US Nat. Acad. Sci., 47, 1956 (1961).
Alpers, D. H., Appel, S. H., and Tomkins, G. M., J. Biol. Chem., 240, 10 (1965).
Lowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R. J., J. Biol. Chem., 193, 265 (1951).
Appel, S. H., Alpers, D. H., and Tomkins, G. M., J. Mol. Biol., 11, 12 (1965).
Krieg, R. H., and Stent, G. S., Mol. Gen. Genetics, 103, 274 (1969).
Krieg, R. H., and Stent, G. S., Mol. Gen. Genetics, 103, 294 (1969).
Capecchi, M. R., Proc. US Nat. Acad. Sci., 58, 1144 (1967).
Bretscher, M. S., J. Mol. Biol., 34, 131 (1968).
Scolnick, E., Tompkins, R., Caskey, T., and Nirenberg, M., Proc. US Nat. Acad. Sci., 61, 768 (1968).
About this article
Cite this article
KANTOR, G., PERSON, S. & ANDERSEN, F. Evidence for a Function for the UAA Codon in vivo. Nature 223, 535–537 (1969). https://doi.org/10.1038/223535a0
Journal of Molecular Biology (1972)
Die Naturwissenschaften (1972)
Journal of Molecular Biology (1971)