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Essay: Synthetic Biology: Repressilator, a Unique Genetic Regulatory Network for Stable Oscillations

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SC462 Elements of Synthetic Biology: Life 2.0

Prof. Manish K Gupta  Spring 2017

DA-IICT

Repressilator

Shreyas bhanderi

ID :- 201401049

Abstract

A cell is composed of many intertwined regulatory and signaling networks. This networks carry

out many essential functions in living cells. The repressilator is a synthetic genetic regulatory

network consisting of a ring-oscillator with three genes, each expressing a protein that represses

the next gene in the loop. The resulting oscillations of repressilator, with typical Periods of hours,

are slower than the cell-division cycle, so the state of the oscillator has to be transmitted from

generation to generation. This arti cial clock displays noisy behavior, possibly because of stochastic

uctuations of its components. By incorporating more speci c control elements, a redesign of the

repressilator might reach (or more optimistically, surpass) the  delity of the biological clocks that

natural selection has produced.

Introduction

Organisms are biochemically dynamic. They are continuously subjected to time-varying conditions

in the form of both extrinsic driving from the environment and intrinsic rhythms generated by

specialized cellular clocks within the organism itself. Relevant examples of the latter are the cardiac

pacemaker located at the sinoatrial node in mammalian hearts. and the circadian clock residing

at the suprachiasmatic nuclei in mammalian brains. These rhythm generators are composed of

thousands of clock cells that are intrinsically diverse but nevertheless manage to function in a

coherent oscillatory state. This is the case, for instance, of the circadian oscillations exhibited by

the suprachiasmatic nuclei, the period of which is known to be determined by the mean period of

the individual neurons making up the circadian clock. The mechanisms by which this collective

behavior arises remain to be understood.

Individual clock cells are known to operate through biochemical networks comprising multiple

regulatory feedback loops. The complexity of these systems has hindered a complete understanding

of natural genetic oscillators. Synthetic genetic networks, on the other hand, o
er an alternative

approach aimed at providing a relatively well controlled test bed in which the functions of natural

gene networks can be isolated and characterized in detail. In this direction, a synthetic biological

oscillator, termed the repressilator, was developed recently in Escherichia coli from a network of

three transcriptional repressors that inhibit one another in a cyclic way. Spontaneous oscillations

were observed in individual cells within a growing culture, although substantial variability and

noise was present among the di
erent cells.

Repressilators were  rst reported in a paper by Michael Elowitz and Stanislas Leibler in 2000 [6].

This network was designed from scratch to exhibit a stable oscillation which is reported via the

expression of green

uorescent protein, and hence acts like an electrical oscillator system with  xed

time periods. The network was implemented in Escherichia coli using standard molecular biology

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methods and observations were performed that verify that the engineered colonies do indeed exhibit

the desired oscillatory behavior.

Figure 1: The repressilator genetic regulatory network.

Michael Elowitz and Stanislas Leibler created a simple mathematical model of transcription regula-

tion. The mathematical model was composed of six molecular species: three mRNA concentrations

and three corresponding repressor protein concentrations. Each species was involved in transcrip-

tion, translation and degradation reactions. Six coupled  rst-order di
erential equations described

the dynamic behaviour of the system. Using the model, the authors predicted what parameters

the stability of the steady state would be dependent on. In particular, the authors used the model

to determine how to induce stable oscillations. Parameters that would favour oscillations were

strong promoters, strong repression of transcription, cooperativity of repressor binding and similar

lifetimes of mRNA and Proteins. The actual synthetic biological system was constructed from nat-

ural components using molecular biological techniques. Two alterations to the natural components

were made to bring the system in line with the parameter space which favours oscillations: strong

but tightly repressable hybrid promoters, and carboxy-terminal tags for the repressor proteins thus

targetting them for protease degradation. A compatible reporter plasmid expressing GFP was also

inserted into the system.

Figure 2: The repressilator circuit with detailed regulation of the promoters. Gi;Mi; Pi and Di

are promoters, mRNA, protein and protein dimer for the gene i, respectively. Index i represents

the target gene (i = 1, 2, 3), whereas k is its repressor (k = 3, 1, 2). Blunt end arrows denote

repression, normal arrows denote activation/production and wavy arrows denote degradation[3].

2

The repressilator consists of three genes connected in a feedback loop, such that each gene represses

the next gene in the loop, and is repressed by the previous gene. Thus, gene G1 is a source of mRNA

M1 (transcription) that codes for the monomer protein P1 produced in the translation process. The

proteins P1 participate in reversible homo-dimerization producing dimers D1, which are repressing

transcription factors (TFs) for the next gene G2. Similarly, gene G2 produces (via transcription,

translation and dimerization) dimer molecules D2, repressing transcription from G3. Finally, TF

molecules D3, produced from gene G3, repress production from G3, completing the cycle ( gure

2). In addition, green

uorescent protein is used as a reporter so that the behavior of the network

can be observed using

uorescence microscopy.

The temporal oscillations of

uorescence occured with a period of approximately 150 minutes,

three times as long as the average cell-division time. Additionally, although sibling cells displayed

correlated GFP levels for a long period of time after septation, there were variations in both period

and amplitude.

Detail description of the topic

The design of the repressilator was guided by two simple mathematical models, one continuous and

deterministic and the other discrete and stochastic.

These models were analyzed to determine the values for the various rates which would yield a

sustained oscillation. It was found that these oscillations were favoured by strong promoters coupled

to e cient ribosome binding sites, tight transcriptional repression (low `leakiness’), cooperative

repression characteristics, and comparable protein and mRNA decay rates.

Figure 3: A continuous simulation of the repressilator.

This analysis motivated two design features which were engineered into the genes: First, to decrease

leakiness the promoter regions were replaced with a tighter hybrid promoter which combined the

 PL promoter with LacL and TetR operator sequences. Second, to reduce the disparity between

the lifetimes of the repressor proteins and the mRNAs, a carboxy terminal tag based on the ssRA

RNA sequence was added at the 3′ end of each repressor gene. This tag is recognized by proteases

which target the protein for degradation. The design was implemented using a low copy plasmid

encoding the repressilator, and the higher copy reporter, which were used to transform a culture

of Escherichia coli.

3

Figure 4: A discrete and stochastic simulation of the repressilator.

Figure 5 describes the repressilator schematically. A repressilator has three genes a, b and c

along with the corresponding proteins they express: A, B and C. These proteins act as repressors,

i.e. they repress or inhibit the rate of expression of the gene next in line. For example, protein

A represses gene b, slowing down the production of protein B. This inhibitory e
ect increases as

the concentration of the protein increases. Similar to A repressing b, B represses c and  nally

C represses a to complete the cycle. Hence it is a negative feedback loop. For example, if we

were to start out with a bit of A and no B or C, and if these genes were not connected, then

the concentrations of each of A, B and C would keep on increasing since the rate of expression is

constant. The only check to this would then be the natural degradation of the proteins (maybe

into their constituent amino acids), which is also always present at a constant rate. However, once

they are connected, a high concentration of A would decrease the expression rate of b, which would

decrease the concentration of B. This would then let c express at a faster rate, which would increase

the concentration of C. This would ultimately result in a checking e
ect on the production of A,

which would have to decrease. Then b would be freer and B would increase, decreasing C and

increasing A again. Hence, the cycle would start once again. Oscillations can be expected, and are

found, in the concentrations of the proteins in the steady state (i.e. after a transient state).

Figure 5: Schematic description of a repressilator.

The repressilator created by Elowitz and Leibler is described thus (see  gure 6). TetR, cl and

LacI are the three proteins that are expressed by their parent genes tetR, cI and lacI. The gene

4

lacI is obtained from E. coli, tetR from the tetracycline-resistance transposon( A transposon is a

discrete piece of DNA that can insert itself into other DNA sequence within the cell. ) Tn10 and

cI from  phage. The protein LacI inhibits the expression of the gene tetR. The protein TetR in

turn inhibits the expression of the gene cI while protein cl inhibits the expression of lacI, thus

completing the cycle. So it is a negative feedback circuit, which could lead to oscillations. A green

uorescent protein (GFP) is used to detect the concentration levels of the repressilator components.

In the left part of the  gure 6 it can be seen that TetR inhibits GFP, so that decrease in intensity

of the GFP as seen by an optical microscope indicates high concentration of TetR. The experiment

performed by Elowitz and Leibler showed oscillations in the concentrations of the proteins with

time periods greater than cell-division time, implying that the state of the oscillator is transmitted

through generations.

Figure 6: Diagram of the repressilator showing the genes and the proteins that make up the

repressilator ( gure from [6] )

Elowitz and Leibler’s mathematical model :

Deterministic: Michaelis-Menten Kinetics The dynamic variables in this model are the

repressor proteins and the mRNA molecules. Gene expression is a combination of two processes:

transcription, in which a gene produces messenger RNA, and translation, in which proteins are pro-

duced from mRNA. Each of the three proteins/mRNA molecules were considered to be identically

behaved. There are six coupled  rst-order di
erential equations.

dmi

dt

= ô€€€mi +

1 + pnj

+
0 (1)

dmi

dt

= ô€€€ (pi ô€€€ mi) (2)

5

The indices i and j run from 1 to 3. Here i =lacI, tetR, cI, while j =cI,lacI,tetR. The quantities pi

and mi are the concentrations of the repressing protein and the mRNA respectively and suitably

normalized (‘concentration’ here means the average copy number per cell).(Copy number means

the average number of molecules of a gene per genome contained in a cell. ) The parameter
+
0

is the rate of production of the protein in absence of the repressing protein. In the presence of a

repressor the rate drops to

1+pnj

+
0 , where the  rst term gives the e
ect of the concentration

of the repressor protein modi ed by the Hill coe cient n, and
0 is the ‘leakiness quotient’ that

describes translation rate independent of the repressor. So the process of gene expression in the

repressilator circuit is divided into two parts: the rate part that is modi ed by the concentration of

the repressor and the other part that is not. The parameter  is the ratio of the decay rates of the

protein and the mRNA. The normalization of the protein and mRNA concentration are thus: mi

is normalized by the translation e ciency which is the average number of proteins produced per

mRNA molecule, while pi is normalized by the quantity Km (called the Michaelis constant) which

is the number of repressor necessary to half-maximally repress a promoter (i:e: an mRNA molecule

which performs translation). The Hill coe cient is a measure of the degree of cooperativity of the

attaching molecules (here the repressors). A Hill coe cient of 1 indicates that the e
ect of binding

a repressor does not depend on the number of repressors already present. A Hill coe cient greater

than one indicates positive cooperativity so that the e
ect of the binding of each new repressor is

enhanced by the number of repressors already bound. A Hill coe cient less than one indicates the

the e
ect of existing repressors decreases the e
ect of each new binding.

Figure 7: Oscillation in the levels of the three repressor proteins in the deterministic case. The inset

shows the normalized autocorrelation function of the  rst protein. The parameter values used by

Elowitz and Leibler were as follows : average translation e ciency= 20 proteins per transcript, Hill

coe cient n = 2, protein half-life= 10 minutes, mRNA half-life= 2 minutes, Km = 40 repressors

per cell ( gure from [6]).

The shaded region in  gure 8 shows the region of parameter space for which oscillations take place.

Stochastic: Gillespie Algorithm Elowitz and Leibler used the Gillespie SSA algorithm to

solve for the stochastic case ( following the Gillespie prescription ). Parameter values used were

chosen keeping in mind that they approximately be similar to those chosen in the deterministic

case. The output was the following  gure.

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Figure 8: Analysis of the stability of the steady state against parameters   and
x Km. Stable

and unstable regions in the   ô€€€
parameter space with respect to the steady state are shown. The

cross mark in the unstable region of the graph corresponds to the parameter values of  gure 7. It

is in the unstable steady state that oscillations occur ( gure from [6]).

It can clearly be seen ( gure 9 ) that there are oscillations which persist, but there is large vari-

ability. As a result, the autocorrelation time is  nite (approximately two periods). So stochasticity

seems to be a nuisance for regular oscillations in the single repressilator both experimentally and

in simulations.

In this model, oscillations are not seen if the Hill coe cient is taken as 1. this means that a single

repressor attached to each transcript carries out the job of repression. This is called non-cooperative

binding. As the Hill coe cient is increased to 2, oscillations are observed for suitable values of

the parameters only if the mRNA level is included. For Hill coe cient 3 or larger, oscillations

take place even if the mRNA level is not included in he analysis. This seems to show that there is

positive cooperativity in the system.

There are several interesting side notes about this elegant yet simple experiment of Elowitz and

Leibler. First, the period of the GFP oscillations was roughly 150 minutes, which is about three

times as long as the length of one E. coli generation under the conditions of the experiment.

However, the two o
spring cells (E. coli reproduces by splitting in two) lost their synchronization

after a little over one generation time. So it can be said that Elowitz and Leibler observed a lot

of noise in their system. Random variation in the levels of repressors and mRNA, as well as other

factors, caused the repressilator to behave somewhat unpredictably.

All in all, these authors were able to produce an oscillating biological clock using the tools of

synthetic biology. The clock wasn’t perfect as it lost synchronization with each new generation,

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Figure 9: Figure 3.3: Oscillation in the levels of the three repressor proteins in the stochas tic case

(y-axis is proteins per cell). The inset shows the normalized autocor relation function of the  rst

protein. A similar set of values of parameters to those of  gure 3.1 were used ( gure from [6]).

and it doesn’t allow for an entire culture of bacteria to blink in sync with one another. However it

is remarkable that this novel system worked as well as it did. The promoters and repressor genes

are parts, each promoter-repressor pair is a device, and the entire clock/reporter can be thought of

as a system.

Examples of simulation experiments of original model

To run a time course simulation on the model as it is available from the BioModels Database [4],

the following steps have to be followed (the execution will lead to Figure 7 and 9 of the original

publication[6]):

1. Import the model identi ed by the Uni ed Resource Identi er [1] urn:miriam:biomodels.db:BIOMD0000000012

(NB: this is the reference for the model encoded in SBML and stored in BioModels Database.

An equivalent reference for the model encoded in CellML and stored in the CellML repository

would be [5] http://models.cellml.org/exposure/6ad4f33a31aa0b9aa81b6558979d72f5.)

2. Select a deterministic method KISAO:0000035 (NB: this is the reference for a term of the

Kinetic Simulation Algorithm Ontology) to run a simulation on that model.

3. Run a uniform time course for the duration of 1000 minutes with an output interval of 1 min.

4. Report the amount of Lactose Operon Repressor, Tetracycline Repressor and Repressor pro-

tein CI against time in a 2D Plot. The result of the simulation is shown in Figure 10.

8

Figure 10: Time-course of the Repressilator model, imported from BioModels

Database (BIOMD0000000012), simulated in COPASI [2], and plotted with Gnuplot

(http://www.gnuplot.info/). The number of repressor proteins lacI, tetR and cI is shown

as a function of the simulated time.

Tools and database

SynBioSS Designer

SynBioSS Designer is a web service to create automatically kinetic model from a Biobricks construc-

tion [Michal Galdzicki et al., 2009], using a set of universal biological rules to get a biomolecular

interactions network.SynBioSS uses the registry of standard biological parts, a database of kinetic

parameters, and both graphical and command-line interfaces to multiscale simulation algorithms.

The International Genetically Engineered Machine (iGEM) Foundation is dedicated to education

and competition, progress of synthetic biology, and the development of an open community and col-

laboration. This organization promotes and fosters scienti c research and education by establishing

and operating the Registry of Standard Biological Parts, a community collection of biological com-

ponents which are used by SynBioSS to obtain the transcriptional units from the Biobricks system.

SynBioSS Designer has the advantage that allows designs and builds distinct genetic circuits from

these Biobricks, obtaining even biochemical and genetic complex buildings upon which could be

able modify some of their characteristics to get the desire reaction network that will describe the

created model, considering the biological rules and laws from which the software is based. SynBioSS

Designer considers the behavior of the individual parts as well as the behavior of the connectivity

9

spatial and temporal of each part, including the biochemical interactions resulting of the system,

so it is accurately, then the biochemical reactions network resulting will become very likely respect

to the reaction generation network that should occurs in vivo underneath biochemical approach.

The types of reactions network generated through the Repressilator corresponding to transcription,

translation, regulation, and induction are stored in the SynBioSS Wiki, so assigns for each reaction

a rate law, according to the number of reactants or the nature of the reaction, and a default kinetic

constant of an appropriate order of magnitude in relation to the nature of the reaction. However,

must pay attention to these values having to seek in di
erent sources as SynBioSS Wiki or relevant

literature to get suitable information pertinent to the system, seeing the dynamic behavior based

on these parameter values. De nitively the reaction network generation will depends on the circuit

design provided through inputs and their properties where several of these can be changed[7].

Figure 11: Table1. The table shows a summary of indputs and their properties which can be

introduced and changed into SynBioss Designer. [7]

Given this information, the Designer begins by extracting all of the transcriptional units from the

sequence of BioBricks. In the Designer approach, a transcriptional unit is de ned as a promoter

followed by an RBS, coding DNA, and one or more terminators. In this case, is developed the

Repressilator, whose shows as far as Designer, a sequence consist of three transcriptional units that

generate a reaction network in accordance with the following reactions. Finally the output is a

reaction network representing all the steps in gene expression and regulation. SynBioss Designer

outputs either a NetCDF or SBML  le [M. Hucka et al., 2003], which can then be loaded in

simulation software such as SynBioSS Desktop Simulator[7].

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BioModels Database

Original Model: BIOMD0000000012.origin

Submitter: Nicolas Le Novre

Submission ID: MODEL6615351360

Submission Date: 13 Sep 2005 12:43:31 UTC

This model describes the deterministic version of the repressilator system. The model is based upon

the equations in Box 1 of the paper [6]; however, these equations as printed are dimensionless, and

the correct dimensions have been returned to the equations, and the parameters set to reproduce

Figure 7 and Figure 9.

Figure 12: Parameters used in BioModels.

Discussion

Elowitz and Leibler built their repressilator in the bacteria E:coli, and used GFP to observe the

presence (or absence) of oscillations. Since single cells had no apparent means to achieve or maintain

synchrony, individual cells were isolated under the microscope and the their

uorescent intensity

was studied as these cells grew into small two-dimensional micro-colonies consisting of hundreds of

progeny cells. The graph shows temporal oscillations in GFP

uorescence intensity with a time-

period of roughly 150 minutes, which happened to be almost three times as large as cell-division

time-scales. Snapshots of a microcolony of bacteria are given in  gure 14, while the

uorescence

intensity of the marked cell against time is given in  gure 13.

11

Figure 13: Oscillations in GFP

uorescence intensity (bars at the bottom indicate septation events)

( gure from [6])

Figure 14: Snapshots of a microcolony of E. coli taken in (a)

uorescence and (b) bright- eld. The

arrows indicate the cell under observation. ( gure from [6])

Looking at the graph ( gure 13), one can see that the time-period of oscillations is around 150

mins (peak-to-peak). The bars at the bottom of the graph show that septation (cell-division) occurs

about three times per oscillation cycle on average, that is, with a time period of about 50 mins. This

conforms to standard cell-division time-periods. Therefore it is seen that the state of the network

is transmitted to its o
springs despite there being noise in the form of stochastic

uctuations in

the dynamics of the cellular clock. However, signi cant di
erences in period and amplitude of

the oscillator were observed in the oscillator output. These di
erences were seen among cells in

di
erent lineages ( descended from di
erent ancestors) or among the cells in one lineage, which are

called siblings (see  gure 15 ).

Elowitz and Leibler conclude that it is possible to design and construct a new arti cial genetic

12

oscillator with new functional properties from generic components. It might then be possible to

attempt to understand the design principles of more complex oscillators such as the circadian

oscillator using the simple repressilator model. However, as opposed to the robust behaviour of

the circadian clock, the behaviour of the repressilator (according to the these experimental results)

seemed to be noisy and variable.

Figure 15: Top left  gure shows phase delays after septation among sibling cells (blue and green)

relative to the reference cell(red). Top right  gure shows that phase is maintained but amplitude

varies greatly after septation. Bottom left  gure is for reduced period (green) and long delay(blue).

Bottom right  gure shows large variations in period and amplitude. The top two  gures and the

bottom left  gure show the variation of oscillation among cells of the same lineage. The bottom

right one shows the variations between cells of di
erent lineages. ( gures from [6])

The repressilator is a milestone of synthetic biology which shows that genetic regulatory networks

which perform a novel desired function can be designed and implemented. Further, the initial ex-

periment gives new appreciation to the circadian clock found in many organisms, as they perform

much more robustly than the repressilator. More recent investigations at the RIKEN Quantitative

Biology Center have found that a single protein molecule could form a temperature independent,

self-sustainable oscillator when it takes chemical modi cations. Repressilators in adapted math-

ematical could potentially aid research in  elds ranging from circadian biology to endocrinology.

They are increasingly able to demonstrate the synchronization inherent in natural biological systems

and the factors that a
ect them.

Elowitz and Leibler are an excellent example of the use of mathematical models to design arti cial

control circuits. These can be either used as components for biotechnology and synthetic biology,

or used to further study and understand properties of naturally evolved control elements.

13

References

[1] Masinter L Berners-Lee T, Fielding R. Uniform resource identi er (uri): Generic syntax, 2005.

[2] Lee C Pahle J Simus N Hoops S, Sahle S. a complex pathway simulator, 2006.

[3] Boris Zhurov Ilya Potapov and Evgeny Volkov. Multi-stable dynamics of the non-adiabatic

repressilator. 2015.

[4] BroicherA Courtot M Donizello M et al Le Novre N, Bornstein B. Biomodels database: a

free, centralized database of curated, published, quantitative kinetic models of biochemical and

cellular systems, 2006.

[5] Hunter PJ Nielsen PF Lloyd CM, Lawson JR. The cellml model repository, 2008.

[6] Stanislas Leibler Michael B. Elowitz. A synthetic oscillatory network of transcriptional regula-

tors. 403:334{338, 2000.

[7] Vernica Llorens-Rico Juan B. Castellanos Perceval Vellosillo, Roberto Tom. Biological processes

studies through software tools: Development and optimization in the simulation of synthetic

biological constructions. 7:23{33, 2013.

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