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Carboxyl-terminal mutants of phage Mu transposase

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An Erratum to this article was published on 01 April 1987

Abstract

A study of the properties of deletion mutants at the 3’ end ofA, the gene encoding the transposase protein of phage Mu, shows that the mutants are defective in the high-frequency non-replicative transposition observed early after Mu infection as well as the high-frequency replicative transposition observed during Mu lytic growth. They show near-normal levels of lysogenization, low frequency transposition and precise excision. The mutants behave as if they are “blind” to the presence of Mu B, a protein whose function is essential for the high frequency of both replicative and non-replicative Mudna transposition. We have sequenced these deletion mutants as well as the amber mutant A 7110 which is known to be defective in replicative transposition.A 7110 maps at the 3’ end of geneA. We suggest that the carboxyl-terminal region of the A-protein is involved in protein-protein interactions, especially with the B-protein. We also show in this study that mutations upstream of the Shine-Dalgarno sequence of geneA and within the preceding genener, perturb the synthesis of A-protein and that higher levels of A-protein cause an inhibition ofA activity.

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An erratum to this article is available at http://dx.doi.org/10.1007/BF02934457.

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Harshey, R.M., Cuneo, S.D. Carboxyl-terminal mutants of phage Mu transposase. J. Genet. 65, 159–174 (1986). https://doi.org/10.1007/BF02931149

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