Most of you have probably heard me going on about my PhD research. A quick overview here though, just so you’re all up to speed. Antibiotic resistance is an increasing problem – I’m sure you’re all aware. New antibiotics are rare discoveries these days, so we need new options. Plasmids are small extrachromosomal pieces of DNA, and often carry antibiotic resistance. They are also often very stably maintained with the bacterial cell, ensuring that this resistance is passed on through generations. The logic goes that if we can prevent the plasmids being inherited, we can remove the antibiotic resistance, and be able to treat the infection again.
For my PhD thesis, I was provided with four plasmids with different stability levels, all of which encoded resistance to ampicillin. My work was to study the effect of this reduction in stability as a model system, and see whether destabilised plasmids would reduce the effectiveness of a cell culture to survive in the presence of ampicillin. I also modified and cloned a series of plasmids with the same stability levels, but with resistance to chloramphenicol.
Generally, it went well, although there were more questions raised than answers provided, which is why it is critical that this work starts again, so we can get the data we need to move forward. Unfortunately it has been over 10 years since I was working regularly on the plasmids, and some have been lost, and others have been contaminated and damaged.
Sophie and I will be working hard over the next few weeks to revive as many of the original plasmids as we can, and recreate the ones that have been lost. It’s off to a good start though – this is a plate of E. coli DH5a cells containing the pOG4 plasmid, proved by the fact that the cells are surviving on a plate containing ampicillin. 1 down… 7 to go…!
