Composite

Part:BBa_K3096046

Designed by: Patrick Mueller, Famke Baeuerle, Jakob Keck, Lina Widerspick   Group: iGEM19_Tuebingen   (2019-10-15)
Revision as of 14:30, 15 October 2019 by Famosa (Talk | contribs)

Fatty acid responsive repression system

The intake of a fatty meal increases the fatty acid availability within the body and therefore their metabolite Acyl-CoA will increase. Long chain Acyl-CoA will bind constitutively expressed FadR and hence inhibits its activity (Feng et al. 2012). FadR is the repressor of the promoter pFad, which regulates the expression of the LsrR repressor, which itself represses the the pLsrR promoter (Federle et al. 2009) regulating the transcription of the plasmid self targeting array. This part represents the whole composite part of the regulatory system used by iGEM Tübingen 2019.

Background

If the bacterium leaves the body, there will be no fatty acids (Acyl-CoA) available. This allows the activity of FadR, which inhibits pFad. Thus, there will be no LsrR and the self targeting array is active. If the self targeting array of the plasmid is active, the Cas3 complex can use it to target the plasmid and degrade it, inducing the degradation of the foreign DNA.

Biology and Usage

The FadR expression system of E.Coli senses Acyl-CoA and activates fatty acid transport genes in vivo (Feng et al. 2012).


Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    INCOMPATIBLE WITH RFC[12]
    Illegal NheI site found at 7
    Illegal NheI site found at 30
    Illegal NheI site found at 902
    Illegal NheI site found at 925
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]


References

  1. Feng Y, Cronan JE. Crosstalk of Escherichia coli FadR with global regulators in expression of fatty acid transport genes. PLoS One. (2012); 7(9):e46275. doi:10.1371/journal.pone.0046275
  2. Federle MJ. Autoinducer-2-based chemical communication in bacteria: complexities of interspecies signaling. Contrib Microbiol. (2009); 16:18–32. doi:10.1159/000219371


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