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Complementary Studies in the Histidine Operon and on Frameshifting: a Compliment to What Roth Has Wrought, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555816810/9781555815387_Chap13-1.gif /docserver/preview/fulltext/10.1128/9781555816810/9781555815387_Chap13-2.gifAbstract:
Explanations for how the set of external Salmonella histidine operon (his) regulatory mutants isolated by John mediated their effects involved the work of many. Several different models for operon origin have been advanced, one being the “selfish operon” hypothesis. Compensatory mutations were isolated, and it was found that these had the mutagenic and other properties of frameshift mutants of opposite sign. One of the major findings from the yeast work was allosuppressors. The secondary mutants that enhanced the effect of the primary frameshift suppressor, termed upf for up-frameshift mutant suppressor, provided an important opening into nmd surveillance. The separation of compensatory mutations very closely linked within the same gene to trpE91 in 1968 and their characteristics of themselves being frameshift mutants were important evidence that trpE91 is a frameshift mutation. There is one additional connection stemming from John, Gerry Fink, and David Botstein doing a sabbatical together in Cold Spring Harbor. They coauthored a paper on yeast suppressor tRNAs with Ray.