The bacteriophage T4 anti‐sigma factor AsiA is not necessary for the inhibition of early promoters <i>in vivo</i>

Pène, Carole; Uzan, Marc

doi:10.1046/j.1365-2958.2000.01787.x

Cited by 26 publications

(22 citation statements)

References 69 publications

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“…When AsiA was described as the ¢rst anti-sigma factor, it was shown that AsiA inactivates the c 70 in vitro to inhibit the transcription of early promoters that carries the conserved 310 and 335 elements. However, recent in vivo work demonstrated that deletion of asiA had no e¡ect on the inhibition of the early promoters [21]. Another line of evidences has suggested that AsiA acts as a switching molecule that alters the promoter preference of c 70 .…”

Section: Discussionmentioning

confidence: 99%

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹

et al. 2002

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Sigma factor binding proteins are involved in modifying the promoter preferences of the RNA polymerase in bacteria. We found the nuclear encoded protein (SibI) that is transported into chloroplasts and interacts specifically with the region 4 of Sig1 in Arabidopsis. SibI and its homologue, T3K9.5 are novel proteins, which are not homologous to any protein of known function. The expression of sibI was tissue specific, light dependent, and developmentally timed. We suggest the transcriptional regulation by sigma factor binding proteins to function in the plastids of higher plant. ß

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Section: Discussionmentioning

confidence: 99%

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹

et al. 2002

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“…The AsiA- 70 interaction is regarded as the pivotal event in the transition between T4 early and middle transcription: in vitro it both inhibits the recognition of most host promoters and early T4 promoters and stimulates T4 middle-mode transcription (180,425,848,849,1104). However, in vivo, defective asiA mutants do not prolong early transcription (858), suggesting that other proteins (i.e., ModA and ModB) turn off most early T4 promoters. MotA is a DNAbinding transcriptional activator protein that binds to the MotA box sequence (Fig.…”

Section: Middle Transcriptionmentioning

confidence: 99%

Bacteriophage T4 Genome

Miller

Kutter

Mosig

et al. 2003

Microbiol Mol Biol Rev

686

801

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SUMMARY Phage T4 has provided countless contributions to the paradigms of genetics and biochemistry. Its complete genome sequence of 168,903 bp encodes about 300 gene products. T4 biology and its genomic sequence provide the best-understood model for modern functional genomics and proteomics. Variations on gene expression, including overlapping genes, internal translation initiation, spliced genes, translational bypassing, and RNA processing, alert us to the caveats of purely computational methods. The T4 transcriptional pattern reflects its dependence on the host RNA polymerase and the use of phage-encoded proteins that sequentially modify RNA polymerase; transcriptional activator proteins, a phage sigma factor, anti-sigma, and sigma decoy proteins also act to specify early, middle, and late promoter recognition. Posttranscriptional controls by T4 provide excellent systems for the study of RNA-dependent processes, particularly at the structural level. The redundancy of DNA replication and recombination systems of T4 reveals how phage and other genomes are stably replicated and repaired in different environments, providing insight into genome evolution and adaptations to new hosts and growth environments. Moreover, genomic sequence analysis has provided new insights into tail fiber variation, lysis, gene duplications, and membrane localization of proteins, while high-resolution structural determination of the “cell-puncturing device,” combined with the three-dimensional image reconstruction of the baseplate, has revealed the mechanism of penetration during infection. Despite these advances, nearly 130 potential T4 genes remain uncharacterized. Current phage-sequencing initiatives are now revealing the similarities and differences among members of the T4 family, including those that infect bacteria other than Escherichia coli. T4 functional genomics will aid in the interpretation of these newly sequenced T4-related genomes and in broadening our understanding of the complex evolution and ecology of phages—the most abundant and among the most ancient biological entities on Earth.

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“…Assigning this function is a long-standing and unresolved question in phage T4 biology (10). It has been recently shown, however, that this transcription shutoff also occurs in the absence of AsiA (11), although the same study confirmed that transcription of E. coli genes is rapidly and strongly inhibited in vivo when AsiA is overproduced.…”

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confidence: 92%

The Escherichia coli RNA Polymerase·Anti-ς70 AsiA Complex Utilizes α-Carboxyl-terminal Domain Upstream Promoter Contacts to Transcribe from a −10/−35 Promoter

Orsini

Kolb

Buc

2001

Journal of Biological Chemistry

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During infection of⅐AsiA to the lacUV5 promoter.In Escherichia coli RNA polymerase, the core enzyme E (subunit composition ␣ 2 ␤␤Ј) associates with the subunit to form the holoenzyme E, the species able to initiate transcription at specific promoter sites on bacterial or phage genomes. The nature and properties of the subunit present in a holoenzyme at a given promoter, together with the ability of the ␣-carboxyl-terminal domain (␣-CTD) 1 to recognize an upstream element of the promoter, determine whether and how often transcription will start at this site (1). These principles are nicely illustrated by the regulation of transcription during the development of phage T4 in E. coli. Here, all the phage genes are transcribed by the host RNA polymerase, the structure and molecular properties of which are modified by phagecoded proteins, resulting in the sequential utilization of early, middle, and late promoters (2, 3). Immediately after infection, T4 early promoters, with their bacterium-like Ϫ10 and Ϫ35 recognition sequences, are transcribed by E 70 , the host holoenzyme harboring 70 , the major host factor. T4 middle promoters contain a Ϫ10 element closely matching the Ϫ10 consensus sequence for 70 , but the Ϫ35 element is replaced by a so-called MotA box, a Ϫ30 binding site for the phage-coded middle transcriptional activator MotA (4, 5). In addition to E 70 and MotA, middle mode transcription also requires the presence of another phage early protein, the anti-factor AsiA (6). Upon binding the MotA box, MotA protein activates recognition of middle promoters by a holoenzyme E 70 ⅐AsiA complex (7, 8). Here, AsiA appears to act as a molecular device that switches 70 from the early to the middle class of T4 promoters. Transcription at late promoters is closely coupled with T4 DNA replication and requires a novel T4-encoded subunit, gp55 (9).Because it is a coactivator of transcription from T4 middle promoters and, simultaneously, a transcription inhibitor of bacterial or T4 early promoters (3), AsiA might also be able to cause the rapid arrest of transcription from early promoters, concomitant with the start of MotA-dependent middle transcription. Assigning this function is a long-standing and unresolved question in phage T4 biology (10). It has been recently shown, however, that this transcription shutoff also occurs in the absence of AsiA (11), although the same study confirmed that transcription of E. coli genes is rapidly and strongly inhibited in vivo when AsiA is overproduced.In vitro transcription studies have helped to outline the mechanism of inhibition by AsiA. This 10-kDa protein binds to region 4.2 of 70 . In the E 70 ⅐AsiA complex, this binding blocks the normal interaction between 70 and the Ϫ35 upstream promoter element (12)(13)(14). Although AsiA strongly inhibits open promoter complex formation and transcription by E 70 from a Ϫ10/Ϫ35 promoter like lacUV5 or the T4 early promoter P15.0, the holoenzyme is resistant to AsiA inhibition at promoters that, like galP1, lack a Ϫ35 consensus motif and conta...

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The bacteriophage T4 anti‐sigma factor AsiA is not necessary for the inhibition of early promoters in vivo

Cited by 26 publications

References 69 publications

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹

Bacteriophage T4 Genome

The Escherichia coli RNA Polymerase·Anti-ς70 AsiA Complex Utilizes α-Carboxyl-terminal Domain Upstream Promoter Contacts to Transcribe from a −10/−35 Promoter

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The bacteriophage T4 anti‐sigma factor AsiA is not necessary for the inhibition of early promoters in vivo

Cited by 26 publications

References 69 publications

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana1

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana1

Bacteriophage T4 Genome

The Escherichia coli RNA Polymerase·Anti-ς70 AsiA Complex Utilizes α-Carboxyl-terminal Domain Upstream Promoter Contacts to Transcribe from a −10/−35 Promoter

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Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹

Novel nuclear‐encoded proteins interacting with a plastid sigma factor, Sig1, in Arabidopsis thaliana¹