Transcription regulatory circuits in bacterial plasmids

2006 ◽  
Vol 34 (6) ◽  
pp. 1072-1074 ◽  
Author(s):  
C.M. Thomas
Keyword(s):  
Gene Regulation ◽  
Plasmid Transfer ◽  
Plasmid Replication ◽  
Plasmid Maintenance ◽  
Plasmid Segregation ◽  
Bacterial Plasmids ◽  
Regulatory Circuits ◽  
Control Plasmid ◽  
Transfer Plasmid

Gene regulation circuits control all aspects of the life of plasmids. This review gives an overview of the current orchestration of the circuits that control plasmid replication, plasmid transfer, plasmid segregation and plasmid maintenance.

scholarly journals A Single Gene on the Staphylococcal Multiresistance Plasmid pSK1 Encodes a Novel Partitioning System

2003 ◽  
Vol 185 (7) ◽  
pp. 2143-2152 ◽  
Author(s):  
Alice E. Simpson ◽  
Ronald A. Skurray ◽  
Neville Firth
Keyword(s):  
Single Gene ◽  
Replication Initiation ◽  
Plasmid Replication ◽  
Rolling Circle ◽  
Plasmid Segregation ◽  
Segregational Stability ◽  
Protein Encoding ◽  
Single Protein ◽  
Encoding Gene ◽  
Postsegregational Killing

ABSTRACT The orf245 gene is located immediately upstream of, and divergently transcribed from, the replication initiation gene, rep, of the Staphylococcus aureus multiresistance plasmid pSK1, and related genes have been found in association with a range of evolutionarily distinct replication genes on plasmids from various gram-positive genera. orf245 has been shown previously to extend the segregational stability of a pSK1 minireplicon. Here we describe an investigation into the basis of orf245-mediated stabilization. orf245 was not found to influence transcription of pSK1 rep, indicating that it is not directly involved in plasmid replication. This was confirmed by demonstrating that orf245 is able to enhance the segregational stability of heterologous theta- and rolling-circle-replicating replicons, suggesting that it encodes a plasmid maintenance function. Evidence inconsistent with postsegregational killing and multimer resolution mechanisms was obtained; however, the intergenic region upstream of orf245 was found to mediate orf245-dependent incompatibility, as would be expected if it encodes a cis-acting centromere-like site. Taken together, these findings implicate active partitioning as the probable basis of the activity of orf245, which is therefore redesignated par. Since it is unrelated to any gene known to play a role in plasmid segregation, it seems likely that pSK1 par potentially represents the prototype of a novel class of active partitioning systems that are distinguished by their capacity to enhance plasmid segregational stability via a single protein-encoding gene.

scholarly journals Regulation of Epstein-Barr Virus Origin of Plasmid Replication (OriP) by the S-Phase Checkpoint Kinase Chk2

2010 ◽  
Vol 84 (10) ◽  
pp. 4979-4987 ◽  
Author(s):  
Jing Zhou ◽  
Zhong Deng ◽  
Julie Norseen ◽  
Paul M. Lieberman
Keyword(s):  
Dna Replication ◽  
Epstein Barr Virus ◽  
Replication Timing ◽  
S Phase ◽  
Plasmid Replication ◽  
Acceptor Site ◽  
Plasmid Maintenance ◽  
Barr Virus ◽  
Amino Terminal ◽  
Epstein Barr

ABSTRACT The Epstein-Barr virus (EBV) origin of plasmid replication (OriP) is required for episome stability during latent infection. Telomere repeat factor 2 (TRF2) binds directly to OriP and facilitates DNA replication and plasmid maintenance. Recent studies have found that TRF2 interacts with the DNA damage checkpoint protein Chk2. We show here that Chk2 plays an important role in regulating OriP plasmid stability, chromatin modifications, and replication timing. The depletion of Chk2 by small interfering RNA (siRNA) leads to a reduction in DNA replication efficiency and a loss of OriP-dependent plasmid maintenance. This corresponds to a change in OriP replication timing and an increase in constitutive histone H3 acetylation. We show that Chk2 interacts with TRF2 in the early G1/S phase of the cell cycle. We also show that Chk2 can phosphorylate TRF2 in vitro at a consensus acceptor site in the amino-terminal basic domain of TRF2. TRF2 mutants with a serine-to-aspartic acid phosphomimetic substitution mutation were reduced in their ability to recruit the origin recognition complex (ORC) and stimulate OriP replication. We suggest that the Chk2 phosphorylation of TRF2 is important for coordinating ORC binding with chromatin remodeling during the early S phase and that a failure to execute these events leads to replication defects and plasmid instability.

scholarly journals Who turned on the lights?: What the regulation of bacterial bioluminescence tells us about this and other bacterial group behaviours

2013 ◽  
Vol 35 (5) ◽  
pp. 18-23 ◽  
Author(s):  
Eric V. Stabb ◽  
Zomary Flores-Cruz
Keyword(s):  
Gene Regulation ◽  
Group Activity ◽  
Bacterial Group ◽  
Bacterial Gene ◽  
Bioluminescent Bacteria ◽  
Regulatory Decision ◽  
Bacterial Bioluminescence ◽  
Regulatory Circuits ◽  
Pheromone Signalling

Luminescence produced by organisms, or ‘bioluminescence’, holds a distinct fascination for humankind, and the study of bacterial bioluminescence has a long history in the field of microbiology. Advances in our understanding of bacterial bioluminescence have in many ways paralleled advances in the field as a whole. Intriguingly, studies of bioluminescent bacteria led to a seminal discovery in bacterial gene regulation and behaviour, because for bacteria, bioluminescence is a group activity. Bioluminescent bacteria communicate using pheromones, and as a result the regulatory decision to induce bioluminescence is only made if a group of bacteria has achieved a dense enough population to allow the build-up of pheromone. More recently, it has become clear that there are complex regulatory circuits governing not only luminescence, but also pheromone signalling itself. These additional layers of regulation pose new questions such as what are bacteria really saying to each other? Understanding regulation may also help answer ancient questions including, what use is luminescence?

scholarly journals Nanoimpact in Plants: Lessons from the Transcriptome

Plants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 751
Author(s):  
Susana García-Sánchez ◽  
Michal Gala ◽  
Gabriel Žoldák
Keyword(s):  
Gene Regulation ◽  
Abiotic Stress ◽  
Comparative Analysis ◽  
Drought Stress ◽  
Stress Responses ◽  
Specific Gene ◽  
Potential Toxicity ◽  
Transcriptional Responses ◽  
Regulatory Circuits ◽  
Pathogen Response

Transcriptomics studies are available to evaluate the potential toxicity of nanomaterials in plants, and many highlight their effect on stress-responsive genes. However, a comparative analysis of overall expression changes suggests a low impact on the transcriptome. Environmental challenges like pathogens, saline, or drought stress induce stronger transcriptional responses than nanoparticles. Clearly, plants did not have the chance to evolve specific gene regulation in response to novel nanomaterials; but they use common regulatory circuits with other stress responses. A shared effect with abiotic stress is the inhibition of genes for root development and pathogen response. Other works are reviewed here, which also converge on these results.

scholarly journals Replication and Control of Circular Bacterial Plasmids

1998 ◽  
Vol 62 (2) ◽  
pp. 434-464 ◽  
Author(s):  
Gloria del Solar ◽  
Rafael Giraldo ◽  
María Jesús Ruiz-Echevarría ◽  
Manuel Espinosa ◽  
Ramón Díaz-Orejas
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Dna Polymerase ◽  
Dna Sequences ◽  
Antisense Rna ◽  
Bacterial Population ◽  
Replication Initiation ◽  
Plasmid Replication ◽  
Genetic Elements ◽  
Bacterial Plasmids

SUMMARY An essential feature of bacterial plasmids is their ability to replicate as autonomous genetic elements in a controlled way within the host. Therefore, they can be used to explore the mechanisms involved in DNA replication and to analyze the different strategies that couple DNA replication to other critical events in the cell cycle. In this review, we focus on replication and its control in circular plasmids. Plasmid replication can be conveniently divided into three stages: initiation, elongation, and termination. The inability of DNA polymerases to initiate de novo replication makes necessary the independent generation of a primer. This is solved, in circular plasmids, by two main strategies: (i) opening of the strands followed by RNA priming (theta and strand displacement replication) or (ii) cleavage of one of the DNA strands to generate a 3′-OH end (rolling-circle replication). Initiation is catalyzed most frequently by one or a few plasmid-encoded initiation proteins that recognize plasmid-specific DNA sequences and determine the point from which replication starts (the origin of replication). In some cases, these proteins also participate directly in the generation of the primer. These initiators can also play the role of pilot proteins that guide the assembly of the host replisome at the plasmid origin. Elongation of plasmid replication is carried out basically by DNA polymerase III holoenzyme (and, in some cases, by DNA polymerase I at an early stage), with the participation of other host proteins that form the replisome. Termination of replication has specific requirements and implications for reinitiation, studies of which have started. The initiation stage plays an additional role: it is the stage at which mechanisms controlling replication operate. The objective of this control is to maintain a fixed concentration of plasmid molecules in a growing bacterial population (duplication of the plasmid pool paced with duplication of the bacterial population). The molecules involved directly in this control can be (i) RNA (antisense RNA), (ii) DNA sequences (iterons), or (iii) antisense RNA and proteins acting in concert. The control elements maintain an average frequency of one plasmid replication per plasmid copy per cell cycle and can “sense” and correct deviations from this average. Most of the current knowledge on plasmid replication and its control is based on the results of analyses performed with pure cultures under steady-state growth conditions. This knowledge sets important parameters needed to understand the maintenance of these genetic elements in mixed populations and under environmental conditions.

Genetic and physical map of a P1 miniplasmid

1982 ◽  
Vol 152 (1) ◽  
pp. 63-71
Author(s):  
S Austin ◽  
F Hart ◽  
A Abeles ◽  
N Sternberg
Keyword(s):  
Physical Map ◽  
Plasmid Replication ◽  
Deletion Mutants ◽  
Plasmid Maintenance ◽  
Bacteriophage P1 ◽  
Daughter Cells ◽  
High Copy Number Plasmid ◽  
Stable Plasmid ◽  
Rep Region ◽  
Stable Unit

The prophage form of bacteriophage P1 is a unit-copy plasmid which is maintained with great fidelity in its Escherichia coli host. The plasmid maintenance functions of P1 are clustered in one region of the genome. An 11.5-kilobase fragment from this region has been cloned into a lambda delta att vector and promotes stable unit-copy plasmid maintenance. The properties of the lambda vector facilitated the isolation of deletion mutants affecting the P1 DNA. Twenty-eight deletion mutants were isolated, and their lesions were mapped by physical techniques. The genetic properties of the mutants with respect to plasmid replication, stability of plasmid maintenance, and ability to exert incompatibility effects against P1 and P7 plasmids were determined. These properties, along with those of several subfragments of the P1 insert cloned into high-copy-number plasmid vectors, allow the construction of an unambiguous genetic and physical map of the maintenance functions. A region of less than 3 kilobases, the rep region, is essential for plasmid replication and contains the incA incompatibility determinant within an 800-base-pair segment. Immediately adjacent to rep is a second region of approximately 3 kilobases which is required for stable plasmid maintenance, but not replication. This region, par, contains a second incompatibility element incB which is approximately 1 kilobase in size. The par region appears to specify equipartition of plasmid copies to daughter cells during cell division.

scholarly journals Crosstalk between vertical and horizontal gene transfer: plasmid replication control by a conjugative relaxase

2017 ◽  
Vol 45 (13) ◽  
pp. 7774-7785 ◽  
Author(s):  
Fabián Lorenzo-Díaz ◽  
Cris Fernández-López ◽  
Rudi Lurz ◽  
Alicia Bravo ◽  
Manuel Espinosa
Keyword(s):  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Plasmid Replication ◽  
Replication Control ◽  
Transfer Plasmid

scholarly journals Discovery of small-molecule inhibitors of multidrug-resistance plasmid maintenance using a high-throughput screening approach

2020 ◽  
Vol 117 (47) ◽  
pp. 29839-29850
Author(s):  
Katelyn E. Zulauf ◽  
James E. Kirby
Keyword(s):  
High Throughput ◽  
High Throughput Screening ◽  
Treatment Options ◽  
Antibiotic Resistance Genes ◽  
Multidrug Resistant ◽  
Replication Initiation ◽  
Plasmid Replication ◽  
Complete Suppression ◽  
Fluorescent Reporter ◽  
Plasmid Maintenance

Carbapenem-resistant Enterobacteriaceae (CRE) are multidrug-resistant pathogens for which new treatments are desperately needed. Carbapenemases and other types of antibiotic resistance genes are carried almost exclusively on large, low-copy-number plasmids (pCRE). Accordingly, small molecules that efficiently evict pCRE plasmids should restore much-needed treatment options. We therefore designed a high-throughput screen to identify such compounds. A synthetic plasmid was constructed containing the plasmid replication machinery from a representativeEscherichia coliCRE isolate as well as a fluorescent reporter gene to easily monitor plasmid maintenance. The synthetic plasmid was then introduced into anE. coliK12tolChost. We used this screening strain to test a library of over 12,000 known bioactive agents for molecules that selectively reduce plasmid levels relative to effects on bacterial growth. From 366 screen hits we further validated the antiplasmid activity of kasugamycin, an aminoglycoside; CGS 15943, a nucleoside analog; and Ro 90-7501, a bibenzimidazole. All three compounds exhibited significant antiplasmid activity including up to complete suppression of plasmid replication and/or plasmid eviction in multiple orthogonal readouts and potentiated activity of the carbapenem, meropenem, against a strain carrying the large, pCRE plasmid from which we constructed the synthetic screening plasmid. Additionally, we found kasugamycin and CGS 15943 blocked plasmid replication, respectively, by inhibiting expression or function of the plasmid replication initiation protein, RepE. In summary, we validated our approach to identify compounds that alter plasmid maintenance, confer resensitization to antimicrobials, and have specific mechanisms of action.

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