RNA Polymerase Elongation Factors

Roberts, Jeffrey W.; Shankar, Smita; Filter, Joshua J.

doi:10.1146/annurev.micro.61.080706.093422

Cited by 99 publications

(138 citation statements)

References 159 publications

(226 reference statements)

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“…NusA is a 55-kDa conserved bacterial protein comprised of an N-terminal domain; the three domains S1, KH1, and KH2 with RNA-binding motifs; and two C-terminal acidic repeat domains AR1 and AR2 (5,6,24,44,48,49,57). In the present study, we identified a recessive substitution mutation in nusA that confers relief of transcriptional polarity (much like missense mutations in rho or nusG) but has no apparent effect on transcription elongation or antitermination in vivo.…”

mentioning

confidence: 71%

“…NusA in E. coli has been best studied as a transcription elongation factor and as a protein required for transcription antitermination in rrn operons and lambdoid phages (6,17,40,44,48). Previous reports have also suggested that NusA can indirectly affect Rho-dependent termination by its influence on the rate of transcription elongation and thereby on transcription-translation coupling (31,58).…”

Section: Discussionmentioning

confidence: 99%

“…Of the various Nus proteins, NusA and NusG also function as general transcription accessory factors, serving to modulate both elongation and termination of transcription elsewhere in the genome (6,40,44,48). The two proteins (both essential for viability in wild-type E. coli) have been reported to exert antagonistic effects on the rate of transcription elongation (increased by NusG and decreased by NusA), and they have also been implicated in the two different processes of transcription termination, namely, intrinsic or factor independent (NusA) and factor dependent (NusA and NusG).…”

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confidence: 99%

“…The NusA protein has been implicated in modulating the rate of transcription elongation (40,44,48) and thus in ensuring the coupling of transcription and translation (58); furthermore, the kinetic coupling model (31) posits that the efficiency of Rho-dependent termination is inversely related to the elongation rate of transcription. Hence, we considered the possibility that the nusA(R258C) mutant is termination-defective because of an inappropriately increased transcription elongation rate in the mutant leading to a mismatch in coupling of RNA polymerase with the pioneer ribosome and with Rho, which would then also explain its suppression by the rpoB8 mutation (Fig.…”

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confidence: 99%

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Compromised Factor-Dependent Transcription Termination in a nusA Mutant of Escherichia coli: Spectrum of Termination Efficiencies Generated by Perturbations of Rho, NusG, NusA, and H-NS Family Proteins

Saxena

Gowrishankar

2011

J Bacteriol

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The proteins NusA and NusG, which are essential for the viability of wild-type Escherichia coli, participate in various postinitiation steps of transcription including elongation, antitermination, and termination. NusG is required, along with the essential Rho protein, for factor-dependent transcription termination (also referred to as polarity), but the role of NusA is less clear, with conflicting reports that it both promotes and inhibits the process. In this study, we found that a recessive missense nusA mutant [nusA(R258C)] exhibits a transcription termination-defective (that is, polarity-relieved) phenotype, much like missense mutants in rho or nusG, but is unaffected for either the rate of transcription elongation or antitermination in phage. Various combinations of the rho, nusG, and nusA mutations were synthetically lethal, and the lethality was suppressed by expression of the N-terminal half of nucleoid protein H-NS. Our results suggest that NusA function is indeed needed for factor-dependent transcription termination and that an entire spectrum of termination efficiencies can be generated by perturbations of the Rho, NusG, NusA, and H-NS family of proteins, with the corresponding phenotypes extending from polarity through polarity relief to lethality.

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confidence: 71%

Section: Discussionmentioning

confidence: 99%

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Compromised Factor-Dependent Transcription Termination in a nusA Mutant of Escherichia coli: Spectrum of Termination Efficiencies Generated by Perturbations of Rho, NusG, NusA, and H-NS Family Proteins

Saxena

Gowrishankar

2011

J Bacteriol

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“…The antitermination activity of N and Q, but not gp39, is enhanced by cell-encoded proteins, including transcription elongation factor NusA, which by itself stimulates termination but reverses its activity to additionally stabilize the TEC in cooperation with N and Q (5, 6). Curiously, the N, Q, gp39, and NusA proteins all target the flexible β flap domain of RNAP (2,4,(7)(8)(9)(10)(11) that forms a part of the RNA exit channel and has been implicated in intrinsic termination and transcription pausing through direct interaction with RNA hairpins (Fig. 1) (3,(12)(13)(14).…”

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confidence: 99%

Distinct pathways of RNA polymerase regulation by a phage-encoded factor

Esyunina

Klimuk

Severinov

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Transcription antitermination is a common strategy of gene expression regulation, but only a few transcription antitermination factors have been studied in detail. Here, we dissect the transcription antitermination mechanism of Xanthomonas oryzae virus Xp10 protein p7, which binds host RNA polymerase (RNAP) and regulates both transcription initiation and termination. We show that p7 suppresses intrinsic termination by decreasing RNAP pausing and increasing the transcription complex stability, in cooperation with host-encoded factor NusA. Uniquely, the antitermination activity of p7 depends on the ω subunit of the RNAP core and is modulated by ppGpp. In contrast, the inhibition of transcription initiation by p7 does not require ω but depends on other RNAP sites. Our results suggest that p7, a bifunctional transcription factor, uses distinct mechanisms to control different steps of transcription. We propose that regulatory functions of the ω subunit revealed by our analysis may extend to its homologs in eukaryotic RNAPs.RNA polymerase | transcription antitermination | transcription pausing | omega subunit | NusA T ranscription promoters and terminators are the main "punctuation marks" that control the expression of individual genes in the genome. In bacteria, transcription termination is an essential regulatory step that determines the relative levels of expression of promoter-proximal and distal genes within operons. Depending on the factors involved, transcription termination in bacteria can be classified as intrinsic (depends on RNAencoded signals) or factor-dependent (requires additional protein factors such as Rho helicase). Intrinsic terminators consist of a G/C-rich hairpin formed in the nascent RNA followed by a downstream oligo(U) tract. During intrinsic termination, RNA polymerase (RNAP) pauses after synthesizing an oligo(U) sequence, accompanied by hairpin formation, leading to subsequent dissociation of the transcription elongation complex (TEC) (1, 2). Despite the relatively simple overall scenario, the exact mechanisms of pausing and hairpin-induced TEC destabilization remain an issue of debate (1, 3).Transcription antitermination is a widespread phenomenon involved in regulation of bacterial and phage operons (2). Transcription antitermination is often mediated by specialized protein factors that target host RNAP and can suppress termination at multiple sites in the operon. The well-studied examples of phage antiterminators include proteins N and Q of Escherichia coli phage λ and the gp39 protein of Thermus thermophilus phage P23-45. These factors suppress RNAP pausing, thus inhibiting the first step of the termination pathway (4-6). The antitermination activity of N and Q, but not gp39, is enhanced by cell-encoded proteins, including transcription elongation factor NusA, which by itself stimulates termination but reverses its activity to additionally stabilize the TEC in cooperation with N and Q (5, 6). Curiously, the N, Q, gp39, and NusA proteins all target the flexible β flap domain of RNAP (2, 4...

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Transcript Elongation and Termination in Bacteria

Richardson

2010

Encyclopedia of Life Sciences

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Ribonucleic acid (RNA) molecules are elongated by the addition of nucleotides to the 3′ end of a nascent RNA by action of RNA polymerase . The substrates are the four ribonucleoside triphosphates. The order of their addition is directed by pairing with an unwound part of the template deoxyribonucleic acid (DNA) strand and is driven by the release of two of the phosphates as pyrophosphate. The rate of addition varies considerably from one nucleotide to the next, but the overall rate is ∼48 nt s −1 along genes encoding proteins, synchronised with the rate of translation. The elongation complex is very stable over most sequences. Termination of transcription can occur at an ‘intrinsic’ terminator – a set of sequences where the complex becomes unstable, or at a Rho‐dependent terminator, where the protein Rho acts on the RNA in the transcription complex to mediate its release. The regulation of expression of genes is controlled in many instances by the action of regulatory terminators (attenuators) or by the function of factors that affect the elongation rate and the action of terminators. Key Concepts: RNA polymerase unwinds ∼15 bp of DNA so that one strand can serve as a template for the assembly of an RNA transcript. The elongation complex of RNA polymerase, DNA and nascent RNA is very stable over most DNA sequences, allowing the synthesis of transcripts that are thousands of nucleotides long. Transcripts encoding protein are elongated with an average rate of 48 nt s −1 , which is synchronous with the rate of translation. The rate of step‐wise addition of nucleotides to the nascent RNA varies considerably from position to position on the DNA. Pauses in the elongation process serves as regulatory points. At the sequences of an intrinsic terminator the elongation complex becomes unstable allowing spontaneous release of a transcript. Termination of transcription is mediated in some cases by action of a factor called Rho, which functions by first binding to an exposed transcript followed by acting on the RNA in a reaction powered by ATP hydrolysis.

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RNA Polymerase Elongation Factors

Cited by 99 publications

References 159 publications

Compromised Factor-Dependent Transcription Termination in a nusA Mutant of Escherichia coli: Spectrum of Termination Efficiencies Generated by Perturbations of Rho, NusG, NusA, and H-NS Family Proteins

Compromised Factor-Dependent Transcription Termination in a nusA Mutant of Escherichia coli: Spectrum of Termination Efficiencies Generated by Perturbations of Rho, NusG, NusA, and H-NS Family Proteins

Distinct pathways of RNA polymerase regulation by a phage-encoded factor

Transcript Elongation and Termination in Bacteria

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