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University of Sheffield/18 July 2008
From 2008.igem.org
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==Conclusion== | ==Conclusion== | ||
| - | As we intend to modify the E-Coli in a way so that its receptor can sense ''V.Cholera & Legionella''. The problem here is | + | As we intend to modify the E-Coli in a way so that its receptor can sense ''V.Cholera & Legionella''. The problem here is both V.Cholera and Legionella have cascading pathways where reactions take place in a series of steps whereas in E.Coli all reactions are simultaneous. So we might have to introduce '''TWO''' plasmids in E.Coli to perform the job. |
Revision as of 20:29, 19 July 2008
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| Low cell density (V.harveyi) |
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| It is seen from the cascading pathway (above) how the gene A-E is not synthesized as repressor gene attaches with the promoter. The pathway starts from autoinducer receptor. |
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| Low cell density (V.Cholera) |
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| The cascading pathway(above) is similiar to the one of V.harveyi but with a slight difference. In V.Cholera HapR i.e. the promoter site is not intact with the repressor gene thus transcription of virulence takes place. |
Conclusion
As we intend to modify the E-Coli in a way so that its receptor can sense V.Cholera & Legionella. The problem here is both V.Cholera and Legionella have cascading pathways where reactions take place in a series of steps whereas in E.Coli all reactions are simultaneous. So we might have to introduce TWO plasmids in E.Coli to perform the job.
