Difference between revisions of "Part:BBa K1954004:Design"
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<br><br>The biosynthetic locus of mutacin III was designed by our team in a form allowing for high-yield and fine-tuned expression of the peptide (Fig. 1). We placed a strong T7 promoter upstream of mutA to obtain high levels of the propeptide, a repressible pTet promoter upstream of the mutBCDP co-transcription unit and an inducible araBAD promoter for the mutT gene, coding for the ATP-binding-cassette-like transporter of mutacin III. All illegal restriction sites were removed from the endogenous sequences by silent mutagenesis. | <br><br>The biosynthetic locus of mutacin III was designed by our team in a form allowing for high-yield and fine-tuned expression of the peptide (Fig. 1). We placed a strong T7 promoter upstream of mutA to obtain high levels of the propeptide, a repressible pTet promoter upstream of the mutBCDP co-transcription unit and an inducible araBAD promoter for the mutT gene, coding for the ATP-binding-cassette-like transporter of mutacin III. All illegal restriction sites were removed from the endogenous sequences by silent mutagenesis. | ||
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===Source=== | ===Source=== |
Revision as of 16:36, 19 October 2016
Nuclease from Staphylococcus aureus
The biosynthetic locus of mutacin III was designed by our team in a form allowing for high-yield and fine-tuned expression of the peptide (Fig. 1). We placed a strong T7 promoter upstream of mutA to obtain high levels of the propeptide, a repressible pTet promoter upstream of the mutBCDP co-transcription unit and an inducible araBAD promoter for the mutT gene, coding for the ATP-binding-cassette-like transporter of mutacin III. All illegal restriction sites were removed from the endogenous sequences by silent mutagenesis.
Assembly Compatibility:
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
Source
Our device was based on the sequence of AF154675.1
Design Notes
All restriction sites were removed by silent mutagenesis.