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Restriction enzymes: the superbug's arch nemesis

 

 

Flesh eating, and drug resistant, bacterial strains are being found more frequently in the UK.

The MRSA strain known as USA300 is nearly untreatable and often lethal, demonstrating how important it is to prevent resistances in the first place, as well as their spread. An international team of scientists have now mapped the structure of a restriction enzyme for the bacteria, a protein which could be used to prevent these resistances to spread.

Bacteria are able to share their genetic blueprint, their DNA, in a process called conjugation. This is a process which resembles sex in higher organisms and is the transfer of a circular piece of DNA from one bacteria to another. This so called plasmid is handed on through a tube-like structure called sex pilus. Through this mechanism a resistant bacteria can pass on its secret of how to survive antibiotic treatment. If one bacteria accumulates many resistance genes it can become a superbug such as MRSA.

For this exchange process the restriction enzymes are needed, which are basically molecular scissors and can chop DNA strands into bits. Originally they might have evolved to protect the bacteria from viruses because it would make the virus' DNA useless once it entered the cell. Nowadays it is used as one of the most important tools in biotechnology.

Due to those properties this enzyme can regulate how much and how fast DNA enters the bacteria. Therefore it can slow down the transfer of genes from another bacteria, and as a result, the accumulation of resistances.

Now the team of scientists from the University of Edinburgh (in collaboration with Universities in England, Poland and France) not only know what the enzyme looks like, but also how it mangles the foreign DNA. This might prove a solution to prevent further resistant superbugs.

Dr David Dryden, who led the study, summarized that: “We have known for some time that these enzymes are very effective in protecting bacteria [...]. Now we have painted a picture of how this occurs, which should prove to be a valuable insight in tackling the spread of antibiotic-resistant superbugs.”

Although the scientist used a harmless strain of Escherichia coli their findings will apply to most other bacteria as well, including potential pathogens.

 

 

Thilo Reich

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