Team:Waterloo

From 2014.igem.org

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<h1 >WELCOME TO iGEM 2014! </h1>
<h1 >WELCOME TO iGEM 2014! </h1>
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'''2014 Project Description:'''
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<b>2014 Project Description:<b>
Waterloo’s 2014 iGEM project aims to remove antibiotic resistance in MRSA populations by using CRISPR and RNA interference systems that target mecA expression. The gene mecA in MRSA is responsible for it’s resistance against beta-lactam antibiotics. CRISPRi and RNAi systems can be incorporated onto a Staphylococcus conjugative plasmid, which would be able to replicate and transfer within a MRSA population, effectively disabling the antibiotic resistant phenotype in the population over time. A beta-lactam antibiotic can then be administered to kill the newly antibiotic-sensitive bacteria.  
Waterloo’s 2014 iGEM project aims to remove antibiotic resistance in MRSA populations by using CRISPR and RNA interference systems that target mecA expression. The gene mecA in MRSA is responsible for it’s resistance against beta-lactam antibiotics. CRISPRi and RNAi systems can be incorporated onto a Staphylococcus conjugative plasmid, which would be able to replicate and transfer within a MRSA population, effectively disabling the antibiotic resistant phenotype in the population over time. A beta-lactam antibiotic can then be administered to kill the newly antibiotic-sensitive bacteria.  

Revision as of 19:16, 15 August 2014


WELCOME TO iGEM 2014!

2014 Project Description: Waterloo’s 2014 iGEM project aims to remove antibiotic resistance in MRSA populations by using CRISPR and RNA interference systems that target mecA expression. The gene mecA in MRSA is responsible for it’s resistance against beta-lactam antibiotics. CRISPRi and RNAi systems can be incorporated onto a Staphylococcus conjugative plasmid, which would be able to replicate and transfer within a MRSA population, effectively disabling the antibiotic resistant phenotype in the population over time. A beta-lactam antibiotic can then be administered to kill the newly antibiotic-sensitive bacteria. To execute this idea, the project was divided into three milestones. The first milestone aims to model the ability of CRISPRi and RNAi to inhibit gene expression in the level one organism, Staphylococcus epidermidis. The second milestone aims to develop an effective conjugative plasmid in Staphylococcus to ensure a proper delivery mechanism for CRISPRi and/or RNAi. Measuring the effectiveness of the conjugative plasmid will allow us to apply our current mathematical models to determine the optimal time periods to apply the antibiotics to the population after the addition of the donor cells. The third milestone would be to evaluate and improve this system for MRSA populations.

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