Difference between revisions of "Part:BBa K3142012"
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<partinfo>BBa_K3142012 parameters</partinfo> | <partinfo>BBa_K3142012 parameters</partinfo> | ||
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+ | ===Engineering Success Made by SZU-China 2021=== | ||
+ | SZU-China team has added quantitative experimental characterization data to an existing Part from the Registry of Standard Biological Parts and documented the experimental characterization on the Part's Main Page on the Registry. | ||
+ | This year,We identified a glucose-sensitive promoter pt-αcrp(BBa_K3142012) that can express subsequent genes at low glucose levels to prevent bacteria from escaping to the outside environment. We added the mazF gene, which encodes an endoribonuclease that will be expressed to suicidal effect when glucose levels are low. We verified our system by inducing expression with different glucose concentrations and observing the survival rate of engineered bacteria and supplemented experimental data for the promoter. | ||
+ | [[File:T--SZU-China--BBa K3838654-GLUK.png]] | ||
+ | |||
+ | As shown in the figure 25, compared with the control group, the growth of the bacteria transformed with the plasmids with the glucose-sensitive suicide switch was basically significantly inhibited, and the lower the glucose concentration in the environment, the more significant the inhibition effect was, and the lower the survival rate was reflected in the experiment. The contrast of the line chart shows the difference between the experimental group and the control group. Based on this, we believe that the glucose sensitive kill switch can work normally. | ||
===Reference=== | ===Reference=== | ||
*William Henry Bothfeld, Grace Kapov, and Keith Tyo. A glucose-sensing toggle switch for autonomous, high productivity genetic control. ACS Synth. 2017, 6(7):1296-1304. | *William Henry Bothfeld, Grace Kapov, and Keith Tyo. A glucose-sensing toggle switch for autonomous, high productivity genetic control. ACS Synth. 2017, 6(7):1296-1304. |
Revision as of 14:12, 6 October 2021
Glucose starvation promoter(PT-αcrp)
PT-αcrp is a Glucose starved promoter,which is response to glucose starvation It can be used to Initiate gene expressing in response to glucose starvation.
Sequence and Features
- 10INCOMPATIBLE WITH RFC[10]Illegal EcoRI site found at 26
- 12INCOMPATIBLE WITH RFC[12]Illegal EcoRI site found at 26
- 21INCOMPATIBLE WITH RFC[21]Illegal EcoRI site found at 26
Illegal BamHI site found at 1 - 23INCOMPATIBLE WITH RFC[23]Illegal EcoRI site found at 26
- 25INCOMPATIBLE WITH RFC[25]Illegal EcoRI site found at 26
- 1000COMPATIBLE WITH RFC[1000]
Engineering Success Made by SZU-China 2021
SZU-China team has added quantitative experimental characterization data to an existing Part from the Registry of Standard Biological Parts and documented the experimental characterization on the Part's Main Page on the Registry. This year,We identified a glucose-sensitive promoter pt-αcrp(BBa_K3142012) that can express subsequent genes at low glucose levels to prevent bacteria from escaping to the outside environment. We added the mazF gene, which encodes an endoribonuclease that will be expressed to suicidal effect when glucose levels are low. We verified our system by inducing expression with different glucose concentrations and observing the survival rate of engineered bacteria and supplemented experimental data for the promoter.
As shown in the figure 25, compared with the control group, the growth of the bacteria transformed with the plasmids with the glucose-sensitive suicide switch was basically significantly inhibited, and the lower the glucose concentration in the environment, the more significant the inhibition effect was, and the lower the survival rate was reflected in the experiment. The contrast of the line chart shows the difference between the experimental group and the control group. Based on this, we believe that the glucose sensitive kill switch can work normally.
Reference
- William Henry Bothfeld, Grace Kapov, and Keith Tyo. A glucose-sensing toggle switch for autonomous, high productivity genetic control. ACS Synth. 2017, 6(7):1296-1304.