Difference between revisions of "Part:BBa K5180777"

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         <center><b>Figure 1: </b>Analysis of Dependent Calprotectin Production</center>
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         <center><b>Figure 1: </b>Calprotectin-Dependent System</center>
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         Figure 1 demonstrates the impact of calprotectin-dependent lysis. Increases in calprotectin concentration result in zinc deficiency, which can then be detected by the ykgMO promoter. When there is a high concentration of zinc, this pathway is suppressed, showing the feedback mechanism of calprotectin in controlling zinc homeostasis.
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         Figure 1 demonstrates the impact of calprotectin-dependent lysis. Increases in calprotectin concentration result in zinc deficiency, which can then be detected by the ykgMO promoter. When there is a high concentration of zinc, this pathway is suppressed, showing the feedback mechanism of calprotectin in controlling the lysis mechanism.
 
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===Usage and Biology===
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        <img src="https://static.igem.wiki/teams/5180/registry/calprotectindependentlysismodeling.jpg" style="width:400px;">
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        <center><b>Figure 2: </b>Mathematical Model of Low and High Calprotectin Concentrations</center>
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        This figure presents a mathematical model showing the relationship between calprotectin concentration and the expression of the lysis gene. At low calprotectin levels, the model predicts minimal lysis gene expression, leading to cell survival. However, as calprotectin concentration increases, the model demonstrates a sharp rise in lysis gene expression, resulting in cell lysis. The model helps illustrate the calprotectin-dependent nature of the proposed lysing mechanism, which is important for dynamic interaction in an intestinal environment.
  
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<span class='h3bb'>Sequence and Features</span>
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<partinfo>BBa_K5180777 SequenceAndFeatures</partinfo>
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===Functional Parameters===
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<partinfo>BBa_K5180777 parameters</partinfo>
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Revision as of 04:18, 2 October 2024


LuxI_LuxR_Plux_rzrz1

This construct integrates the luxI/luxR quorum sensing system to drive the inducible production of the rzrz01 lysis gene in Escherichia coli. Modeled after the quorum sensing system of Vibrio fischeri, this design enables cell-to-cell communication, ultimately triggering cell lysis. When the luxI gene synthesizes the signaling molecule acyl homoserine lactone (AHL), it binds to the LuxR regulator. The LuxR-AHL complex then interacts with the Plux promoter, activating the transcription of the rzrz01 lysis gene. This results in controlled self-lysis of the bacterial cells in response to AHL accumulation.

Images and Figures

Figure 1: Calprotectin-Dependent System
Figure 1 demonstrates the impact of calprotectin-dependent lysis. Increases in calprotectin concentration result in zinc deficiency, which can then be detected by the ykgMO promoter. When there is a high concentration of zinc, this pathway is suppressed, showing the feedback mechanism of calprotectin in controlling the lysis mechanism.
Figure 2: Mathematical Model of Low and High Calprotectin Concentrations
This figure presents a mathematical model showing the relationship between calprotectin concentration and the expression of the lysis gene. At low calprotectin levels, the model predicts minimal lysis gene expression, leading to cell survival. However, as calprotectin concentration increases, the model demonstrates a sharp rise in lysis gene expression, resulting in cell lysis. The model helps illustrate the calprotectin-dependent nature of the proposed lysing mechanism, which is important for dynamic interaction in an intestinal environment.