The 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, 25 000 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.
Working small RNAs!
Constructed small RNAs that can downregulate antibiotic resistance. Read more
Improved existing parts
Improved standard plasmid backbones from the low copy pSB4X series. Read more
Characterized several promoters and their respective promoter strengths. Read more
Helped other teams
Our BioBricks have been requested by many iGEM teams. Read more
Constructed several new BioBricks and characterized them. Read more
Had a great summer while working with our iGEM project. Read more
We have developed a modular screening system and protocol for finding silencing sRNAs against arbitrary genes. Using this, we have found strongly silencing sRNAs against a clinical antibiotic gene and lowered the minimal inhibatory concentration tenfold in resistant bacteria.
We 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 done as it turned out that the common registry pSB4 backbones all have faulty copy number regulation, while we needed low copy backbones for out project.
Proteins with a visible intrinsic color are the simplest possible reporters in molecular biology. Most iGEMers are familiar with the Red Flourescent Protein (RFP), but there are many other colors available among the organisms of the world. We have characterized and submitted new chromoproteins, allowing multiplexed colorful reporters.