Regulation of transcription from tandem and convergent promoters

Horowitz, Heidi; Platt, Terry

doi:10.1093/nar/10.18.5447

Cited by 61 publications

(25 citation statements)

References 24 publications

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“…2D and 3D). This is consistent with the observation that when the trp and lacUV5 promoters were placed in opposition to one another, in vitro transcriptional interference resulted only under abnormal conditions (low purine nucleoside triphosphate concentrations [29]). At least under some conditions, in vivo transcription from tandem promoters can lead to RNA polymerase collisions and termination by the trailing polymerase (42), though among the spacings tested this effect was seen only when the two promoters were 83 bp apart, and in pvuIIM the two transcript starts are separated by half that distance.…”

Section: Discussionsupporting

confidence: 91%

Role and Mechanism of Action of C · Pvu II, a Regulatory Protein Conserved among Restriction-Modification Systems

et al. 2000

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The PvuII restriction-modification system is a type II system, which means that its restriction endonuclease and modification methyltransferase are independently active proteins. The PvuII system is carried on a plasmid, and its movement into a new host cell is expected to be followed initially by expression of the methyltransferase gene alone so that the new host's DNA is protected before endonuclease activity appears. Previous studies have identified a regulatory gene (pvuIIC) between the divergently oriented genes for the restriction endonuclease (pvuIIR) and modification methyltransferase (pvuIIM), with pvuIIC in the same orientation as and partially overlapping pvuIIR. The product of pvuIIC, C ⅐ PvuII, was found to act in trans and to be required for expression of pvuIIR. In this study we demonstrate that premature expression of pvuIIC prevents establishment of the PvuII genes, consistent with the model that requiring C ⅐ PvuII for pvuIIR expression provides a timing delay essential for protection of the new host's DNA. We find that the opposing pvuIIC and pvuIIM transcripts overlap by over 60 nucleotides at their 5 ends, raising the possibility that their hybridization might play a regulatory role. We furthermore characterize the action of C ⅐ PvuII, demonstrating that it is a sequence-specific DNA-binding protein that binds to the pvuIIC promoter and stimulates transcription of both pvuIIC and pvuIIR into a polycistronic mRNA. The apparent location of C ⅐ PvuII binding, overlapping the ؊10 promoter hexamer and the pvuIICR transcriptional starting points, is highly unusual for transcriptional activators.The bacterial type II restriction-modification systems include a DNA modification methyltransferase (MTase) and a restriction endonuclease (REase), both of which act independently on the same DNA sequence (65). The REase cleaves duplex DNA sequences in the absence of sequence-specific DNA modification by the MTase. These systems can defend bacterial cells against viral infection, although other functional roles have also been proposed (45). Restriction-modification systems have provided an important focus for studies of molecular recognition. Biochemical and crystallographic analyses are yielding significant insights into the mechanisms of sequence recognition and catalytic activity of these proteins (3,18,50,66).

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Section: Discussionsupporting

confidence: 91%

Role and Mechanism of Action of C · Pvu II, a Regulatory Protein Conserved among Restriction-Modification Systems

et al. 2000

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“…We find it plausible that induction of P2 and P1 may occur through dislodgement of a repressor sitting on these promoters by RNAP molecules proceeding from upstream promoters. Previous reports of RNAP colliding into a protein bound to a downstream position on DNA showed that in some cases, RNAP may be halted by the bound protein through a roadblock mechanism (35)(36)(37)(38), whereas in others, the elongating complexes are able to bypass the roadblock, probably by dislodgement of the blocking protein (39)(40)(41)(42). Two factors contribute to readthrough by the RNAP: (i) when multiple RNAP complexes transcribe in tandem, trailing elongation complexes cooperate with the leading complex to bypass the block (39,43), and (ii) nascent RNA-translating ribosomes, which closely follow transcribing RNAP, provide a supplemental impelling force that facilitates readthrough of roadblocks in vivo (44,45).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Internal Promoters in a Zinc-Responsive Operon Is Influenced by Transcription from Upstream Promoters

Napolitano

Rubio

Camargo

et al. 2013

Journal of Bacteriology

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In the cyanobacterium Anabaena sp. strain PCC 7120 (also known as Nostoc sp. strain PCC 7120), a zinc-responsive operon (all4725-all4721) has been described, which contains 4 distinct promoters. The two most upstream ones bind Zur with high affinity, whereas the other two do not or do so with a very low affinity. In this paper, a detailed characterization of the four promoters is presented, showing that all four were induced by metal depletion, and they were constitutively derepressed in a zur mutant, despite the two downstream promoters not being direct targets for this regulator. Crucially, induction by metal depletion of the two downstream promoters was abrogated when transcription initiated at the upstream promoters was interrupted by a polar insertion midway in the operon. In contrast, insertion of a nitrogen-responsive promoter at a roughly similar position provoked the two downstream promoters to adopt a regulatory pattern mimicking that of the inserted promoter. Thus, regulation of the two downstream promoters is apparently influenced by transcription from promoters upstream. Evidence is presented indicating that the activity of the two downstream promoters is kept basal in Anabaena by repression. A regulatory model compatible with these results is proposed, where promoters controlled by repression in bacterial operons may be subjected to a hierarchical regulation depending on their position in the operon. According to this model, internal promoters may respond to stimuli governing the activity of promoters upstream by an indirect regulation and to specific stimuli by a direct regulation.

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“…The earlier publications that have influenced our understanding of the mechanisms involved are in vivo studies on convergent promoters by Ward and Murray [61], an in vitro study on promoters arranged both convergently and in-tandem by Horowitz and Platt [62] and, in particular, the in vivo study of a convergent promoter pair by Elledge and Davis [63]. In eukaryotes, pioneering in vivo work has been performed by the Proudfoot laboratory [11] on promoter pairs that are arranged tandemly.…”

Section: How Does Transcriptional Interference Work?mentioning

confidence: 99%

Transcriptional interference – a crash course

2005

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The term 'transcriptional interference' (TI) is widely used but poorly defined in the literature. There are a variety of methods by which one can interfere with the process or the product of transcription but the term TI usually refers to the direct negative impact of one transcriptional activity on a second transcriptional activity in cis. Two recent studies, one examining Saccharomyces cerevisiae and the other Escherichia coli, clearly show TI at one promoter caused by the arrival of a transcribing complex initiating at a distant promoter. TI is potentially widespread throughout biology; therefore, it is timely to assess exactly its nature, significance and operative mechanisms. In this article, we will address the following questions: what is TI, how important and widespread is it, how does it work and where should we focus our future research efforts? What is transcriptional interference?In this article, we wish to define transcriptional interference (TI) specifically as the suppressive influence of one transcriptional process, directly and in cis on a second transcriptional process. Our definition of TI (see Glossary) excludes the kind of interference that results from the following: (i) the binding of a repressor to its operator overlapping a promoter [1]; (ii) promoter modification, such as methylation [2]; (iii) hindering the progress of an elongating RNA polymerase (RNAP) by DNA-bound obstacles (other than a second RNAP) [3]; (iv) the inactivation of RNAP by RNA regulators [4]; (v) the insulation of an enhancer site [5]; and (vi) RNA interference (RNAi) in which the product of one transcriptional unit interferes with the half-life of the product of a second transcriptional unit [6]. We exclude from our definition of TI examples whereby transcription interferes directly with a cellular activity rather than with transcription associated with cellular activity (e.g. the interference with chromosome replication in Saccharomyces cerevisiae as a result of transcription across its site of initiation [7]). We also exclude those cases of 'negative interference' whereby one transcriptional process, directly and in cis, enhances rather than suppresses a second transcriptional process, such as the fortuitous positioning of a gene within an active chromatin domain [8], chromatin remodelling that promotes intergenic transcription [9] and transcriptional coupling in which a promoter is activated by the activity of an upstream divergent promoter [10].TI is often asymmetric and results from the existence of two promoters, the strong (aggressive) promoter reducing the expression of the weak (sensitive) promoter (Figure 1). These promoters can be either: (i) convergent promoters directing converging transcripts that overlap for at least part of their sequence ( Figure 1a); (ii) tandem promoters, one upstream of the other but transcribing in the same direction, with their transcripts possibly but not necessarily overlapping ( Figure 1b); or (iii) overlapping promoters, either divergent, convergent or tandem, in whi...

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Regulation of transcription from tandem and convergent promoters

Cited by 61 publications

References 24 publications

Role and Mechanism of Action of C · Pvu II, a Regulatory Protein Conserved among Restriction-Modification Systems

Role and Mechanism of Action of C · Pvu II, a Regulatory Protein Conserved among Restriction-Modification Systems

Regulation of Internal Promoters in a Zinc-Responsive Operon Is Influenced by Transcription from Upstream Promoters

Transcriptional interference – a crash course

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