Team:Uppsala University
From 2012.igem.org
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<b>Working smallRNA!</b><br> | <b>Working smallRNA!</b><br> | ||
- | Constructed smallRNA downregulating antibiotic resistance.<br><b><a href="https://2012.igem.org/Team:Uppsala_University/ | + | Constructed smallRNA downregulating antibiotic resistance.<br><b><a href="https://2012.igem.org/Team:Uppsala_University/Translational">Read more</a> </b> |
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<b>Improved existing part</b><br> | <b>Improved existing part</b><br> |
Revision as of 03:58, 27 September 2012
Project descriptionThe first half of the 20th century saw a revolution in the treatment of one of the major curses of mankind: pathogenic microorganisms. After the invention of first sulfa and later penicillin, through the fourties, fifties and sixties a large number of antibiotic drugs were quickly found. The age when many bacterial infections meant life-threatening epidemics were soon forgotten, as illnesses could now be cured by a few days with antibiotics. During the sixties and seventies, bacterial infections was largely considered to be a solved problem in the western world, and drug researchers turned to other areas. However, evolution is a more powerful force than one can imagine, and soon the bacterias got the upper hand. In later years, it has become clear that bacterial resistance is spreading at a faster rate than anyone could imagine. Between the seventies and late nineties, no new classes of antibiotics were launched, while usage of antibiotics continued at an ever increasing rate. This created an ideal enviroment for antibiotic resistance to spread. Today, it is estimated that, in the EU alone, 25 00 patients die yearly of multidrug resistant infections, which also increase health care costs by over 1.5 billion euro per year. Antibiotic research has been given higher priority in academic institutions over the last decade, but it is clear that drug development is and has been stalled for a long time. But do we really have to give up classic antibiotic drugs? Team Uppsala University 2012 begs to differ. We believe that new knowledge about bacterial regulatory mechanisms can enable us to once again turn resistant bacteria sensitive to classic antibiotics. This summer, we decided to show it. |
Achivements
Working smallRNA!
Constructed smallRNA downregulating antibiotic resistance. Read more Improved existing part Improved standard plasmid backbones from the 4 series. Read more Cool new biobricks Made several biobricks and new applications for them, demonstrated how they worked and characterized them. Read more Helped other teams. By sending several of oour constructed biobrick parts to other teams. Read more Characterization of promotors Measured several different promotors to gain better understand of promotor choice. |
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Silencing sRNAWe have developed a modular screening system and protocol for finding silencing sRNA:s against arbitrary genes. Using this, we have found a strongly silencing sRNA:s against a clinical antibiotic gene and lowered the minimary inhibatory concentration five-fold in resistant bacteria. |
New BackbonesWe have constructed a range of new standard low copy backbones, and variants with built-in lacIq repression for tight control of toxic genes, thermosensitivity and FRT sites for removing resistance cassettes. This work was induced as it turned out that the common registry pSB4 backbones all have a faulty copy number regulation, while we needed low copy backbones for out project. |
ChromoproteinsProteins with an visible intrinsic color are the simplest possible reporters i molecular biology. Most iGEM:ers are familiar with the Red Flourescent Protein (RFP), but there are many other colors aviable among all organism of the world. We have characterized and submitted new chromoproteins, allowing multiplexed colorful reporters. |