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<p><h5>Collaboration with University of Göttingen</h5></p> | <p><h5>Collaboration with University of Göttingen</h5></p> | ||
− | <p>The University of Göttingen helped us testing the cytotoxic activity of Minicolicin (nehmen wir das jetzt???) in other organisms than <i>E. coli</i>. Specifically, <i>(Organismus)</i> was transformed with Minicolicin without mutation (mCol<sub>WT</sub>) and with mutation (@Jonas: welche Mutation ist das?) (mCol<sub>Mut</sub>) under control of the T7 promoter BioBrick <a href="http://parts.igem.org/Part:BBa_K525998">BBa_K525998</a> on the BioBrick backbone pSB1A3.<br> | + | <p>The University of Göttingen helped us testing the cytotoxic activity of Minicolicin (nehmen wir das jetzt???) in other organisms than <i>E. coli</i>. Specifically, <i>(Organismus)</i> was transformed with Minicolicin without mutation (mCol<sub style="font-size:50%;">WT</sub>) and with mutation (@Jonas: welche Mutation ist das?) (mCol<sub style="font-size:50%;">Mut</sub>) under control of the T7 promoter BioBrick <a href="http://parts.igem.org/Part:BBa_K525998">BBa_K525998</a> on the BioBrick backbone pSB1A3.<br> |
The <i>(Organismus)</i> cells were transformed via electroporation with the mCol variants and cultivated on LB-Agar plates supplemented with ampicillin. This procedure was performed in dublicate. I order to ensure that pSB1A3 is suitable for amplification in <i>(Organismus)</i>, original pSB1A3 was also tested.<br> | The <i>(Organismus)</i> cells were transformed via electroporation with the mCol variants and cultivated on LB-Agar plates supplemented with ampicillin. This procedure was performed in dublicate. I order to ensure that pSB1A3 is suitable for amplification in <i>(Organismus)</i>, original pSB1A3 was also tested.<br> | ||
− | No significant difference in colony amount on each LB-Agar plate was obseverd between the two Minicolicin constructs: mCol<sub>WT<sub> transformed cells yielded 220±20 colonies and mCol<sub>Mut<sub> cells yielded 200±50 colonies(mean of the dublicate with standard deviation).</p> | + | No significant difference in colony amount on each LB-Agar plate was obseverd between the two Minicolicin constructs: mCol<sub style="font-size:50%;">WT</sub> transformed cells yielded 220±20 colonies and mCol<sub style="font-size:50%;">Mut</sub> cells yielded 200±50 colonies(mean of the dublicate with standard deviation).</p> |
<p><h5>Collaboration with RWTH Aachen</h5></p> | <p><h5>Collaboration with RWTH Aachen</h5></p> | ||
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Revision as of 16:09, 10 October 2016
Collaborations
Collaboration with University of Göttingen
The University of Göttingen helped us testing the cytotoxic activity of Minicolicin (nehmen wir das jetzt???) in other organisms than E. coli. Specifically, (Organismus) was transformed with Minicolicin without mutation (mColWT) and with mutation (@Jonas: welche Mutation ist das?) (mColMut) under control of the T7 promoter BioBrick BBa_K525998 on the BioBrick backbone pSB1A3.
The (Organismus) cells were transformed via electroporation with the mCol variants and cultivated on LB-Agar plates supplemented with ampicillin. This procedure was performed in dublicate. I order to ensure that pSB1A3 is suitable for amplification in (Organismus), original pSB1A3 was also tested.
No significant difference in colony amount on each LB-Agar plate was obseverd between the two Minicolicin constructs: mColWT transformed cells yielded 220±20 colonies and mColMut cells yielded 200±50 colonies(mean of the dublicate with standard deviation).
Collaboration with RWTH Aachen
Since our iGEM team as well as the team of the RWTH Aachen worked with an expanded genetic code via amber supression, we exchanged our knowledge on this topic. Furthermore they tested the incorporation efficiency of our orthogonal tRNA OMT-RS pair with the "Expanded Genetic Code Measurement Kit". In exchange we modeled the molecular dynamics of Subtilisin E with the nnAA O-(2-nitrobenzyl)-l-tyrosine (ONBY) at the specified position.