Figure 1. Convergent transcription in the scbA-scbR gene regulatory network.

(A) Schematic of the promoter regions for pA and pR, and RNAP footprint at the respective promoters. (B) The scbA-scbR gene regulatory network. Convergent promoter pA-pR drive expression of genes scbA (shown in red) and scbR (shown in black) present on the opposite DNA strands (shown by black lines) to give rise to full-length transcripts a and r (RNA denoted by curved lines) and short truncated RNA (denoted by dashed-curved lines) respectively. Transcriptional Interference model: Collision between elongating RNAPs and between an elongating RNAP and a stationary RNAP at the opposing promoter causes transcriptional termination and results in the generation of short truncated transcripts (dashed-curved lines) from promoters pA and pR respectively. Full-length transcripts a and r result when elongating RNAPs escape collision. Antisense Regulation: Hybrid RNA complexes formed between full-length a and r RNA result in translational inhibition or mRNA degradation. Protein ScbR (R) can repress transcription from pA and pR (indicated by blunt arrows) by binding to operator sites O_A and O_R adjacent to promoters pA and pR respectively. Only full-length transcripts a and r are translated to protein ScbA (A) and ScbR (R). The intracellular γ-butyrolactone SCB1 (denoted by C_i) is produced from glycerol derivatives and β-keto acid by the enzymatic action of γ-butyrolactone synthase ScbA. SCB1 forms complex with ScbR (C_iR) to sequester its repressive effect. SCB1 diffuses out of the cell in to the extracellular environment and vice versa (denoted by C_e). The reactions are numbered according to equations in Table 1.