Team:ULB-Brussels/Modelling/2A-Peptid

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$~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ \newcommand{\MyColi}{{\small Mighty\hspace{0.12cm}Coli}} \newcommand{\Stabi}{\small Stabi}$ $\newcommand{\EColi}{\small E.coli} \newcommand{\SCere}{\small S.cerevisae}\\[0cm] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ \newcommand{\PI}{\small PI}$ $\newcommand{\Igo}{\Large\mathcal{I}} \newcommand{\Tgo}{\Large\mathcal{T}} \newcommand{\Ogo}{\Large\mathcal{O}} ~$ Example of a hierarchical menu in CSS

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-Du nouveau pour comparer avec et sans p2A? Yes, now we get it!




- Université Libre de Bruxelles -


2A Peptide


$\newcommand{\Tox}{\small Tox} \newcommand{\AnTox}{\small Anti\hspace{0.08cm} Tox} \newcommand{\EColi}{\small E.Coli}$

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. $\EColi$ can insert other plasmids, containing the $\Tox$ and the $\AnTox$ 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 $\AnTox$ genes, but another promoter, pBAD, controls the transcription of the $\Tox$ gene, situated in another plasmid than the $\PI$ $\&$ the $\AnTox$ genes.

The problem with the classical system is that if there are a lot of mutations or a lot of heterogeneity in the $\EColi$ 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 $\EColi$.

With our $\MyColi$ system, the sub-producing bacteria are eliminated from the bioreactor because these $\EColi$ don't produce the $\PI$ in sufficient quantity (the $\PI$ is produced at same rate than the $\AnTox$, thanks to the $2A$ $Peptid$). Because the presence of the $p2A$ is necessary with $\MyColi$, the losses can be divided in two classes: (1) bacteria without cleavage of p2A $\hspace{0.1cm}\&\hspace{0.1cm}$ (2) bacteria killed by TA system, when there's more $\Tox$ than $\AnTox$.

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Conclusion >