This was a hypothesis paper. Already, in a separate (but related) paper, I had shown through arguments how it was likely that ninety percent of the genes in the E.coli genome (responsible for the expression of less than ten percent of the total protein produced despite being responsible for expression of ninety percent of the types of protein produced) transcribe in a manner induced by the passage of the replication fork. In this paper, I dealt with the transcription of genes that are unlikely to be regulated by replication. I argued that with many genes which belong to this variety, transcription itself can either aid fresh transcription, or even induce further transcription, through a detailed analysis of the known relationships between transcription and DNA supercoiling. Briefly, using the bidirectional cause-effect relationship between supercoiling and transcription, I demonstrate how it is necessary that RNA polymerases must be organized to transcribe together in batteries of contiguously-placed transcription complexes, and contiguously-placed genes supporting such transcription complexes, for the transcription-driven supercoiling created by one polymerase to be annulled and annihilated by the polymerase immediately behind it, in a battery of transcribing polymerases. This is critical because there aren’t enough topoisomerase enzymes in the cell which can handle the quantum of transcription simultaneously occurring within the cell, for enzymes to neutralize all transcription-driven supercoiling. Further, for negative supercoiling-dependent promoters, I also showed how transcription must be periodic and also how this periodicity may be altered by linking the transcription-driven negative supercoiling propagating upstream of any transcribing polymerase to the next initiation of transcription at the promoter vacated by such a polymerase, by differentially-limiting such propagation of supercoiling through the designer artifice of upstream acting sequences binding to transcriptional activators. The mechanisms explained in this paper also illuminate events occurring downstream of any battery of transcribing polymerases; in particular, the breakthrough transcription occurring past any cruciform structure located at the end of any gene. I showed how poorer frequency of transcriptional initiation could (almost counter-intuitively) produce more breakthrough transcription past a cruciform structure than highly frequent transcription, through an entirely logical argument deriving from transcription driven positive supercoiling occurring downstream of a polymerase and its effects on melting of cruciform structures. The greatest joy of publishing this paper came from the chance discovery that it had been reviewed by the scientist who had first proposed transcription-driven supercoiling as a possibility (because the journal’s review showed the scientist’s signature at the bottom of the review)!

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