Team:Imperial College London/M2/EncapsulationRationale
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=[[Image:II09_Thumb_m2.png|40px]]<font size='5'><b>Module 2 - Encapsulsation Overview</b></font>= | =[[Image:II09_Thumb_m2.png|40px]]<font size='5'><b>Module 2 - Encapsulsation Overview</b></font>= | ||
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- | <td width=" | + | <td width="20%"><center><a href="https://2009.igem.org/Team:Imperial_College_London/M2"><b>Module 2 Overview</b></a></center></td> |
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Revision as of 13:49, 8 October 2009
Module 2 - Encapsulsation Overview
Encapsulation Rationale
In nature, encapsulation pathways such as spore formation, aliginate biosynthesis and colanic acid production all share one common feature: they require a large number of genes. For this reason, we decided that the best way encapsulate our chassis was via the modulation of an existing pathway.
E.coli naturally produces a harmless acid resistant polymer known as colanic acid. By tapping into the pathway that initiates colanic acid biosynthesis, we can turn on its production via the modulation of a gene called RcsB.
In nature, colanic acid acts as a binding agent between individual cells over which a biofilm can be formed. While colanic acid itself is harmless, biofilm formation is associated with the production of a number of virulence factors. To prevent biofilm formation from occuring, we have tapped into a second pathway such that our cells become locked into colanic acid production. The gene responsible for preventing biofilm formation is a transcription factor called YgiV.
In nature, colanic acid is associated with but not attached to the cell surface. To facilitate whole cell encapsulation, we have modified a third pathway to fix the colanic acid to the surface of the cell. This involves an enzyme called Rfal.