Team:NYMU-Taipei/Modeling/Overview

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=Overview=
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==System description==
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== Overview ==
 
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This year, our team targets to tackle a challenging problem all over the world - CCD, colony collapse disorder by creating a special kind of ''E. coli''. Our project can mainly be separated into four main parts – prevention, sensing and killing, suicuding, and safety.
 
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In the first part prevention, monosidase is used, which can inhibit Nosema polarfilament development. This part is mainly done by experiment.
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Our model can be generally divided into two sections:
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In the second part sensing and killing, it can further divide into three parts – entrance, sensing, and killing. In entrance part, we use beads (encapsulation) to make it easy for our bacteria getting into the bee. For sensing part, we choose ROS-induced promoters, which can be triggered due to the increase concentration of active transcription factor(OxyR or SoxR). As for killing part, microbial peptides defensin and abaecin are used to pierce Nosema cell wall and then let it be bursted.
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*'''Circuit design'''
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:The first section of our model describes the regulation of Beecoli’s system, which mainly consists of three parts:
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Here we are interested in the relationship between concentration ROS, active transcription factor and ROS-induced promoters’ open strength. Furthermore, we also want to know the lag time between sensing the invasion and the production of the killing protein to see if the device can save the bees from being killed by Nosema. As a result, we use sensor model to attain this goal.
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::1. Sensing: In this part, we describe how a constitutive promoter enhances the expressed level of activator OxyR. Results are presented as a graph showing changes in OxyR concentration as time progress.
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However, the spread of E.coli from bee to bee is also another important factor influencing the efficiency of killing Nosema. Consequently, epidemic model is applied to see the relationship between Nosema infection and E, coli treatment.
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::2. Killing protein production: In this part, we describe the regulation pathway of killing protein production after AhpCp senses Nosema invasion. Results are presented as a graph showing changes in killing protein concentration as time progress after sensing promoter is triggered, which explains whether killing protein can eliminate Nosema ceranae timely.
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In the third part suiciding, ethanol is used to make bees which are fail to survive after E.coli loses to kill Nosema to suicide itself. Because this part should not be easily opened, otherwise, bees will under the threat of being killed all the time even without the presence of Nosema, we add several terminals behind promoter. Here, ethanol model is used to simulate how many terminals do we need as a threshold.
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::3. Ethanol production: In this part, we describe the regulation pathway of ethanol production after AhpCp senses Nosema invasion. Results are presented as a graph showing changes in ethanol concentration as time progress after sensing promoter is triggered, which explains whether ethanol eliminates a sick bee timely when killing protein fails to kill Nosema, and that ethanol won’t kill a bee if it is cured in time.
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The last part is safety issue. Since it may be disastrous to the environment if E.coli escapes from bee’s body, we want E.coli to be killed once it leaves bees’ body. Light sensor is used to achieve this goal.
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:In this system, OxyR senses changes in ROS level and regulate other circuits with promoter AhpCp, by enhancing its expression it regulates killing protein production and ethanol production more keenly. Killing protein and ethanol production effects an infected bee alternatively when the bee is in different Nosema invasion stages.
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*'''Effect of Beecoli on the bee colony'''
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:The second section of our model describes the system in which Nosema ceranae and Beecoli infect the subjected colony by an epidemic model. Results are presented as graphs showing population changes as time progress. In addition, there is a graph showing what capsule dosage and infection severity will result in which survival rate of the bee colony eventually for practical purpose.
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:This part of the model is based on the circuit’s efficiency discussed on the first section of our model.
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==Contributions==
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#Our models for the circuit help the wet lab to choose biobricks for when designing the circuit.
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##To learn how the constitutive promoter regulating OxyR production was chosen, click here.
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##To learn how the regulators CI and LuxR were chosen in AMP production circuit, click here.
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##To learn how the terminator set in ethanol producing circuit was chosen, click here.
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#Our model for the synergistic effect of ''Nosema ceranae'' and Beecoli on an invaded colony provides a guideline for those who want to put our cure into practice.
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To learn about the tug of war between ''Nosema ceranae'' and Beecoli over the bees, and how many capsules should be fed to a bee colony in different infection stages, [[click here]].
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==Innovations==
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#We describe transcription and translation process separately and subsidized promoter strength with PoPS, constructing a realistic dynamic system rather than the old one described by possibilities. [[To learn about this mechanism, click here.]]
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#We describe positive and negative regulation by combining the experimental data with hill equation.[[To learn about this mechanism, click here2.]]
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==Parameters and Reference==
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The promoter strengths used in our circuit model is provided by promoter testing conducted by our wet lab and partly from partregistry.
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Statistics regarding how the capsules carry Beecoli into a bee’s midgut is provided by our wet lab experiment. The population growth rate is provided by previous research on ''Nosema ceranae'' influences on ''Apis Mellifera'' done by the experts.
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{{:Team:NYMU-Taipei/Footer}}

Latest revision as of 03:07, 29 October 2013

National Yang Ming University


Contents

Overview

System description

Our model can be generally divided into two sections:

  • Circuit design
The first section of our model describes the regulation of Beecoli’s system, which mainly consists of three parts:
1. Sensing: In this part, we describe how a constitutive promoter enhances the expressed level of activator OxyR. Results are presented as a graph showing changes in OxyR concentration as time progress.
2. Killing protein production: In this part, we describe the regulation pathway of killing protein production after AhpCp senses Nosema invasion. Results are presented as a graph showing changes in killing protein concentration as time progress after sensing promoter is triggered, which explains whether killing protein can eliminate Nosema ceranae timely.
3. Ethanol production: In this part, we describe the regulation pathway of ethanol production after AhpCp senses Nosema invasion. Results are presented as a graph showing changes in ethanol concentration as time progress after sensing promoter is triggered, which explains whether ethanol eliminates a sick bee timely when killing protein fails to kill Nosema, and that ethanol won’t kill a bee if it is cured in time.
In this system, OxyR senses changes in ROS level and regulate other circuits with promoter AhpCp, by enhancing its expression it regulates killing protein production and ethanol production more keenly. Killing protein and ethanol production effects an infected bee alternatively when the bee is in different Nosema invasion stages.
  • Effect of Beecoli on the bee colony
The second section of our model describes the system in which Nosema ceranae and Beecoli infect the subjected colony by an epidemic model. Results are presented as graphs showing population changes as time progress. In addition, there is a graph showing what capsule dosage and infection severity will result in which survival rate of the bee colony eventually for practical purpose.
This part of the model is based on the circuit’s efficiency discussed on the first section of our model.

Contributions

  1. Our models for the circuit help the wet lab to choose biobricks for when designing the circuit.
    1. To learn how the constitutive promoter regulating OxyR production was chosen, click here.
    2. To learn how the regulators CI and LuxR were chosen in AMP production circuit, click here.
    3. To learn how the terminator set in ethanol producing circuit was chosen, click here.
  2. Our model for the synergistic effect of Nosema ceranae and Beecoli on an invaded colony provides a guideline for those who want to put our cure into practice.

To learn about the tug of war between Nosema ceranae and Beecoli over the bees, and how many capsules should be fed to a bee colony in different infection stages, click here.

Innovations

  1. We describe transcription and translation process separately and subsidized promoter strength with PoPS, constructing a realistic dynamic system rather than the old one described by possibilities. To learn about this mechanism, click here.
  2. We describe positive and negative regulation by combining the experimental data with hill equation.To learn about this mechanism, click here2.

Parameters and Reference

The promoter strengths used in our circuit model is provided by promoter testing conducted by our wet lab and partly from partregistry.

Statistics regarding how the capsules carry Beecoli into a bee’s midgut is provided by our wet lab experiment. The population growth rate is provided by previous research on Nosema ceranae influences on Apis Mellifera done by the experts.

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