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Team:ULB-Brussels/Modelling/2A-Peptid
From 2014.igem.org
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The objective of $\Stabi$ is to stabilize the presence of the plasmids that contain the $\PI$ gene sequence. | The objective of $\Stabi$ is to stabilize the presence of the plasmids that contain the $\PI$ gene sequence. | ||
| - | $E.Coli$ can insert other plasmids, containing the $Tox$ and the $A-Tox$ genes. | + | $\small E.Coli$ can insert other plasmids, containing the $Tox$ and the $A-Tox$ genes. |
These two proteins are produced at same rate (contitutive promoter: T7) and the $\PI$ is independently produced in this classical system.</p> | These two proteins are produced at same rate (contitutive promoter: T7) and the $\PI$ is independently produced in this classical system.</p> | ||
The objective of $\Stabi$ is a little bit different: The T7 promoter iniciates the transcription of the $\PI$ $\&$ the $A-Tox$ genes, but another promoter, pBAD, controls the transcription of the $Tox$ gene, situated in another plasmid than the $\PI$ $\&$ the $A-Tox$ genes. </p> | The objective of $\Stabi$ is a little bit different: The T7 promoter iniciates the transcription of the $\PI$ $\&$ the $A-Tox$ genes, but another promoter, pBAD, controls the transcription of the $Tox$ gene, situated in another plasmid than the $\PI$ $\&$ the $A-Tox$ genes. </p> | ||
| - | The problem with the classical system is that if there are a lot of mutations or a lot of heterogeneity in the E.Coli population, the $PI$ is not produced at high rate. In a bioreactor built to product a special kind of $\PI$, this system's not optimal because there're $\PI$ losses, especially if the $\PI$ gene sequence is long or if the $\PI$ is cumbersome for $E.Coli$. | + | The problem with the classical system is that if there are a lot of mutations or a lot of heterogeneity in the $\small E.Coli$ population, the $\PI$ is not produced at high rate. In a bioreactor built to product a special kind of $\PI$, this system's not optimal because there're $\PI$ losses, especially if the $\PI$ gene sequence is long or if the $\PI$ is cumbersome for $\small E.Coli$. |
</tr> | </tr> | ||
Revision as of 12:44, 20 September 2014
$~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ \newcommand{\MyColi}{{\small Mighty\hspace{0.12cm}Coli}} \newcommand{\Stabi}{\small Stabi}$ $\newcommand{\EColi}{\small E.coli} \newcommand{\SCere}{\small S.cerevisae}\\[0cm] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ \newcommand{\PI}{\small PI}$ $\newcommand{\Igo}{\Large\mathcal{I}} \newcommand{\Tgo}{\Large\mathcal{T}} \newcommand{\Ogo}{\Large\mathcal{O}} ~$
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Now we're ready to compare our $\MyColi$ with the usual $\Stabi$ system. The objective of $\Stabi$ is to stabilize the presence of the plasmids that contain the $\PI$ gene sequence. $\small E.Coli$ can insert other plasmids, containing the $Tox$ and the $A-Tox$ genes. These two proteins are produced at same rate (contitutive promoter: T7) and the $\PI$ is independently produced in this classical system. The objective of $\Stabi$ is a little bit different: The T7 promoter iniciates the transcription of the $\PI$ $\&$ the $A-Tox$ genes, but another promoter, pBAD, controls the transcription of the $Tox$ gene, situated in another plasmid than the $\PI$ $\&$ the $A-Tox$ genes. The problem with the classical system is that if there are a lot of mutations or a lot of heterogeneity in the $\small E.Coli$ population, the $\PI$ is not produced at high rate. In a bioreactor built to product a special kind of $\PI$, this system's not optimal because there're $\PI$ losses, especially if the $\PI$ gene sequence is long or if the $\PI$ is cumbersome for $\small E.Coli$. -Du nouveau pour comparer avec et sans p2A? Yes, now we get it!
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- Université Libre de Bruxelles -
