Team:Stockholm/Modelling/Suitable model

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Latest revision as of 02:15, 28 October 2010

Choosing a proper model for LacI/allolactose dynamics

With the details mentioned in the introduction, the first step should be to prepare a proper model for allolactose/lactose dynamics. The reason for this is that binding of allolactose to LacI inhibits it from binding to the lac operator, which will result in gene expression. [http://www.ncbi.nlm.nih.gov/pubmed/12719218 Yildirim N et al. (2002)] proposed a mathematical model for lac operon induction in E. coli. The details that they considered in their model are what we are looking for: external lactose, internal lactose, conversion of lactose to allolactose and glucose, interaction of allolactose with LacI and mRNA. Since LacI also acts as a repressor in our plasmid expression vector, it is reasonable to use the same model as [http://www.ncbi.nlm.nih.gov/pubmed/12719218 Yildirim N et al. (2002)].

We start by a short reminder about the lac operon in E. coli. The lac operon is responsible for transport and metabolism of lactose in E. coli. It has a promoter site and three structural genes (lacZ, lacY and lacA). Availability of external lactose and glucose regulates this operon. In the absence of lactose the lacI gene, which is always expressed, codes for the LacI repressor and represses the expression the of lac operon. When lactose is available again for the bacteria in the absence of glucose, allolactose (a β-galactosidase side reaction) binds to the repressor and prevents the repressor from binding to the lac operon operator. This will result in production of high levels of LacZ (β-galactosidase), LacY (β-galactoside permease) and LacA; the latter is not interesting in our case. LacZ and LacY expression will lead to more production of Allolactose (a metabolite of lactose).

The Faculty of Science at Stockholm University

Swedish Vitiligo association (Svenska Vitiligoförbundet)

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-=== Choosing proper model for LacI/allolactose dynamics ===
+=== Choosing a proper model for LacI/allolactose dynamics ===
 <div align="justify">With the details mentioned in the introduction, the first step should be to prepare a proper model for allolactose/lactose dynamics. The reason for this is that binding of allolactose to LacI inhibits it from binding to the ''lac'' operator, which will result in gene expression. [http://www.ncbi.nlm.nih.gov/pubmed/12719218 Yildirim N ''et al.'' (2002)] proposed a mathematical model for lac operon induction in ''E. coli''. The details that they considered in their model are what we are looking for: external lactose, internal lactose, conversion of lactose to allolactose and glucose, interaction of allolactose with LacI and mRNA. Since LacI also acts as a repressor in our plasmid expression vector, it is reasonable to use the same model as [http://www.ncbi.nlm.nih.gov/pubmed/12719218 Yildirim N ''et al.'' (2002)].
-We start slowly by talking a little about the ''lac'' operon in ''E. coli. The ''lac'' operon is responsible for transport and metabolism of lactose in ''E. coli''. It has a promoter site and three structural genes (''lacZ'', ''lacY'' and ''lacA''). Availability of external Lactose and Glucose regulates this operon. In the absence of Lactose the ''lacI'' gene, which is always expressed, codes for the LacI repressor and represses the expression the of ''lac'' operon. When Lactose is available again for the bacteria in the absence of glucose, Allolactose (a β-galactosidase side reaction) binds to the repressor and prevents the repressor from binding to the ''lac'' operon operator. This will result in production of high levels of LacZ (β-galactosidase), LacY (β-galactoside permease) and LacA; the latter is not interesting in our case. LacZ and LacY expression will lead to more production of Allolactose (a metabolite of lactose).
+We start by a short reminder about the ''lac'' operon in ''E. coli''. The ''lac'' operon is responsible for transport and metabolism of lactose in ''E. coli''. It has a promoter site and three structural genes (''lacZ'', ''lacY'' and ''lacA''). Availability of external lactose and glucose regulates this operon. In the absence of lactose the ''lacI'' gene, which is always expressed, codes for the LacI repressor and represses the expression the of ''lac'' operon. When lactose is available again for the bacteria in the absence of glucose, allolactose (a β-galactosidase side reaction) binds to the repressor and prevents the repressor from binding to the ''lac'' operon operator. This will result in production of high levels of LacZ (β-galactosidase), LacY (β-galactoside permease) and LacA; the latter is not interesting in our case. LacZ and LacY expression will lead to more production of Allolactose (a metabolite of lactose).
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