Mini-P1 plasmid replication: the autoregulation-sequestration paradox.

D K Chattoraj; R J Mason; S H Wickner

doi:10.1016/0092-8674(88)90468-0

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Mini-P1 plasmid replication: the autoregulation-sequestration paradox.

D K Chattoraj·R J Mason·S H Wickner

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Abstract

It has been proposed that the initiator protein RepA is rate limiting for mini-P1 plasmid replication, and that the role of the plasmid copy number control locus is to sequester the initiator and thus reduce replication. This proposal appears inconsistent with the observation that RepA is autoregulated, since the protein lost by sequestration should be replenished. A resolution of this autoregulation-sequestration paradox is possible if the sequestered RepA, unavailable for replication, is still available for promoter repression. We demonstrate that RepA binds to the control locus and to the promoter region simultaneously, causing the intervening DNA to loop. DNA looping could provide the requisite mechanism by which RepA bound to the control locus might exert repression.

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DNA Helicases DNA Replication DNA, Bacterial DNA-Binding Proteins Escherichia coli Gene Expression Regulation Microscopy, Electron Nucleic Acid Conformation Plasmids Promoter Regions, Genetic Proteins Repressor Proteins Trans-Activators Transcription Factors Viral Proteins Journal Article

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D K Chattoraj, R J Mason, S H Wickner. 1988-02-26. Mini-P1 plasmid replication: the autoregulation-sequestration paradox.. https://doi.org/10.1016/0092-8674(88)90468-0

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