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. 1974 Oct;120(1):245–252. doi: 10.1128/jb.120.1.245-252.1974

Promoter-Like Mutation Affecting HPr and Enzyme I of the Phosphoenolpyruvate:Sugar Phosphotransferase System in Salmonella typhimurium1

J Christopher Cordaro a, R Philip Anderson a,2, E Wayne Grogan Jr a,3, Donald J Wenzel a,4, Michael Engler a, Saul Roseman a
PMCID: PMC245757  PMID: 4608878

Abstract

A promoter-like mutation, ptsP160, has been identified which drastically reduces expression of the genes specifying two proteins, HPr and enzyme I, of the phosphoenolpyruvate:sugar phosphotransferase system (PTS) in Salmonella typhimurium. This mutation lies between trzA, a gene specifying susceptibility to 1,2,4-triazole, and ptsH, the structural gene for HPr. It leads to a loss of active transport of those sugars that require the PTS for entry into the cell. Pseudorevertants of strains carrying this promoter-like mutation have additional lesions very closely linked to ptsP160 by transduction analysis and are noninducible for HPr and enzyme I above a basal level. Presumably, strains carrying ptsP160 are defective in the normal induction mechanism for HPr and enzyme I, and the pseudorevertants derived from them result from second-site initiation signals within or near this promoter-like element. The induction of HPr and enzyme I above their noninduced levels apparently is not required for transport of at least one PTS sugar, methyl α-d-glucopyranoside, since this sugar is taken up by the pseudorevertants at the same rate as by the wild type. The existence of a promoter-like element governing the coordinate inducibility of both HPr and enzyme I suggests that ptsH and ptsI constitute an operon. Wild-type levels of a sugar-specific PTS protein, factor III, are synthesized in response to the crr+ gene in both a ptsP160 strain and its pseudorevertants; this suggests that the crr+ gene has its own promoter distinct from ptsP.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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