scholarly journals Hypothesis: hypersensitive plasmid copy number control for ColE1

1996 ◽  
Vol 70 (1) ◽  
pp. 135-145 ◽  
Author(s):  
M. Ehrenberg
Keyword(s):  
Copy Number ◽  
Plasmid Copy Number ◽  
Plasmid Copy ◽  
Copy Number Control

scholarly journals Plasmid copy number control: an ever-growing story

2002 ◽  
Vol 37 (3) ◽  
pp. 492-500 ◽  
Author(s):  
Gloria Del Solar ◽  
Manuel Espinosa
Keyword(s):  
Copy Number ◽  
Plasmid Copy Number ◽  
Plasmid Copy ◽  
Copy Number Control

scholarly journals Genetic dissection of centromere function.

1993 ◽  
Vol 13 (6) ◽  
pp. 3156-3166 ◽  
Author(s):  
I G Schulman ◽  
K Bloom
Keyword(s):  
Chromosome Segregation ◽  
Copy Number ◽  
Artificial Chromosome ◽  
Plasmid Copy Number ◽  
Genetic Dissection ◽  
Negative Effects ◽  
Plasmid Copy ◽  
Complex Cells ◽  
Copy Number Control

A system to detect a minimal function of Saccharomyces cerevisiae centromeres in vivo has been developed. Centromere DNA mutants have been examined and found to be active in a plasmid copy number control assay in the absence of segregation. The experiments allow the identification of a minimal centromere unit, CDE III, independently of its ability to mediate chromosome segregation. Centromere-mediated plasmid copy number control correlates with the ability of CDE III to assemble a DNA-protein complex. Cells forced to maintain excess copies of CDE III exhibit increased loss of a nonessential artificial chromosome. Thus, segregationally impaired centromeres can have negative effects in trans on chromosome segregation. The use of a plasmid copy number control assay has allowed assembly steps preceding chromosome segregation to be defined.

Noise in a minimal regulatory network: plasmid copy number control

2001 ◽  
Vol 34 (1) ◽  
pp. 1-59 ◽  
Author(s):  
Johan Paulsson ◽  
Måns Ehrenberg
Keyword(s):  
Copy Number Variation ◽  
Rate Constants ◽  
Copy Number ◽  
Time Delays ◽  
Plasmid Copy Number ◽  
Plasmid Copy ◽  
Copy Number Control ◽  
Plasmid R1 ◽  
Number Variation ◽  
Control Curves

1. Introduction 22. Plasmid biology 32.1 What are plasmids? 32.2 Evolution of CNC: cost and benefit 42.3 Plasmids are semi-complete regulatory networks 62.4 The molecular mechanisms of CNC for plasmids ColE1 and R1 62.4.1 ColE1 72.4.2 R1 72.5 General simplifying assumptions and values of rate constants 93. Macroscopic analysis 113.1 Regulatory logic of inhibitor-dilution CNC 113.2 Sensitivity amplification 123.3 Plasmid control curves 133.4 Multistep control of plasmid ColE1: exponential control curves 143.5 Multistep control of plasmid R1: hyperbolic control curves 163.6 Time-delays, oscillations and critical damping 184. Mesoscopic analysis 204.1 The master equation approach 204.2 A random walker in a potential well 234.3 CNC as a stochastic process 244.4 Sensitivity amplification 264.4.1 Single-step hyperbolic control 264.4.2 ColE1 multistep control can eliminate plasmid copy number variation 284.4.3 Replication backup systems – the Rom protein of ColE1 and CopB of R1 294.5 Time-delays 304.5.1 Limited rate of inhibitor degradation 304.5.2 Precise delays – does unlimited sensitivity amplification always reduce plasmid losses? 324.6 Order and disorder in CNC 334.6.1 Disordered CNC 344.6.2 Ordered CNC: R1 multistep control gives narrowly distributed interreplication times 344.7 Noisy signalling – disorder and sensitivity amplification 374.7.1 Eliminating a fast but noisy variable 384.7.2 Conditional inhibitor distribution: Poisson 394.7.3 Increasing inhibitor variation I: transcription in bursts 404.7.4 Increasing inhibitor variation II: duplex formation 414.7.5 Exploiting fluctuations for sensitivity amplification: stochastic focusing 444.7.6 A kinetic uncertainty principle 454.7.7 Disorder and stochastic focusing 464.7.8 Do plasmids really use stochastic focusing? 474.8 Metabolic burdens and values of in vivo rate constants 485. Previous models of copy number control 495.1 General models of CNC 495.2 Modelling plasmid ColE1 CNC 495.3 Modelling plasmid R1 CNC 526. Summary and outlook: the plasmid paradigm 537. Acknowledgements 568. References 56This work is a theoretical analysis of random fluctuations and regulatory efficiency in genetic networks. As a model system we use inhibitor-dilution copy number control (CNC) of the bacterial plasmids ColE1 and R1. We chose these systems because they are simple and well-characterised but also because plasmids seem to be under an evolutionary pressure to reduce both average copy numbers and statistical copy number variation: internal noise.

scholarly journals The evolution of coercive policing in genetically mixed groups: the case of plasmid copy number control

2016 ◽  
Author(s):  
Kyriakos Kentzoglanakis ◽  
Sam P. Brown ◽  
Richard A. Goldstein
Keyword(s):  
Reproductive Success ◽  
Computational Model ◽  
Copy Number ◽  
Genetic Relatedness ◽  
Group Performance ◽  
Plasmid Copy Number ◽  
System Level ◽  
Evolution Of Cooperation ◽  
Plasmid Copy ◽  
Copy Number Control

AbstractPolicing is a widespread mechanism regulating cooperation in both human and animal social groups. Policing can promote the evolution and maintenance of cooperation among non-relatives by tying the reproductive success of individuals to the efficiency and success of the group. In this paper, we investigate the evolution of reproductive policing using a multi-scale computational model inspired by the copy number control system of conjugative bacterial plasmids. Our results show that the repression of competition through policing can evolve across a very broad range of migration (plasmid conjugation) rates, improving system-level performance and bringing efficiency gains to the group beyond those achievable by pure self-restraint. Reproductive policing acts to increase genetic relatedness by reducing variation in group size which, in turn, reduces the heterogeneity of the plasmid population. When among-group migration is high, coercive policing strategies are favoured, characterized by high levels of policing coupled with relatively lower obedience. Coercive policing strategies preferentially limit the reproduction of rival lineages while, at the same time, maintaining effective collective reproductive control.Author SummaryThe emergence and maintenance of cooperation is a topic of great importance in evolutionary biology. The evolution of cooperation has been explained in the context of kin selection when there is sufficient genetic relatedness among interacting individuals. When there is insufficient relatedness, the presence of alternative mechanisms, such as mutual policing, can promote the evolution and maintenance of cooperation by tying the reproductive success of individual to the efficiency and success of the group. In this paper, we investigate the evolution of reproductive policing using an agent-based computational model inspired by a simple and elegant biological example: replication control among conjugative plasmids, a class of molecular symbionts of bacterial hosts. Our results show that the repression of competition through policing evolves and improves plasmid group performance beyond levels achievable by self-restraint, across a very broad range of migration rates. Under conditions of high migration (frequent conjugation), we observe the evolution of coercive policing strategies that limit the reproduction of rival lineages by investing disproportionately in policing relative to their obedience to the policing trait.

scholarly journals Genetic dissection of centromere function

1993 ◽  
Vol 13 (6) ◽  
pp. 3156-3166
Author(s):  
I G Schulman ◽  
K Bloom
Keyword(s):  
Chromosome Segregation ◽  
Copy Number ◽  
Artificial Chromosome ◽  
Plasmid Copy Number ◽  
Genetic Dissection ◽  
Negative Effects ◽  
Plasmid Copy ◽  
Complex Cells ◽  
Copy Number Control

A system to detect a minimal function of Saccharomyces cerevisiae centromeres in vivo has been developed. Centromere DNA mutants have been examined and found to be active in a plasmid copy number control assay in the absence of segregation. The experiments allow the identification of a minimal centromere unit, CDE III, independently of its ability to mediate chromosome segregation. Centromere-mediated plasmid copy number control correlates with the ability of CDE III to assemble a DNA-protein complex. Cells forced to maintain excess copies of CDE III exhibit increased loss of a nonessential artificial chromosome. Thus, segregationally impaired centromeres can have negative effects in trans on chromosome segregation. The use of a plasmid copy number control assay has allowed assembly steps preceding chromosome segregation to be defined.

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