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The SOS response: how bacteria deal with damaged DNA

The views expressed are those of the author and are not necessarily those of Scientific American.


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DNA is important stuff. It’s present in all living organisms on the planet (or ‘almost all’ if you wish to remain friends with virologists) and contains the information required to produce and organise the proteins within a cell. If the DNA is damaged, the cell will very quickly find itself in danger. In multicellular organisms the result of one cell going haywire is so catastrophic that the usual response to anything other than very simple DNA damage is for the damaged cell to commit honourable suicide.

On the left, human ovary cells. On the right, the cells undergoing apoptosis, or programmed cell death. Image from wikimedia commons, in reference two

In unicellular bacteria, the results of DNA damage only affect the cell in question, and as the internal organisation of the cell is more flexible the cell can get away with slightly more shoddy DNA repair. In some cases this can even be an advantage; changes to the DNA may result in new genes or gene combinations which may be of benefit to the bacteria.

The bacterial response to DNA damage is known as the SOS response. There are two main proteins involved – one, LexA, to keep the response switched off while the cell is healthy and the other, RecA, to turn it on when DNA damage occurs. In normal healthy cells the LexA protein binds to a certain section of the bacterial DNA called the ‘SOS box’ which codes for over 50 genes while RecA floats around the cell looking for damaged DNA. If it finds any, it binds to it and stimulates the breaking of the LexA protein. The SOS box genes are therefore released and the proteins that deal with DNA damage can be made.

Factors that can activate the bacterial SOS response. Image from reference 1. Click image for a readable version!

Although all the SOS genes are eventually activated, they are not all turned on at once. The first proteins to be made are those that repair simple DNA damage such as problems with single nucleotides. Then more LexA is made; and if the problem has been solved then no further genes are required. If there is still significant DNA damage the cell starts to produce low fidelity DNA polymerases. High fidelity DNA polymerases are used to replicate DNA, and to produce proteins from the genetic code. These low fidelity ones are the equivalent of cowboy builders, slapping together any old nucleotides to get the DNA back into one piece.

These low fidelity polymerases may seem a bit slapdash, but because of the low fidelity they can mend pieces of DNA that are so damaged that they would cause the high fidelity ones to stall, or get stuck. At first glance it might seem unfortunate that the DNA cannot be repaired more accurately, but these low fidelity polymerases are actually a secret weapon. By making sloppy, error-prone patches in the DNA they increase the mutation rate. If the bacteria is undergoing major DNA damage then there’s a chance that these mutations may throw up something useful. It’s a sort of insta-evolution for times of stress.

As well as trying to repair damaged DNA, the SOS response is involved in a number of other exciting responses to cell damage. In E. coli the SOS box turns on proteins that promote cell hibernation and dormancy. It can also cause to the cells to form biofilms, and in some bacteria it turns on the production of antibiotic resistance genes.

In view of this some interesting work has been done on blocking the bacterial SOS response. While this won’t kill the bacteria, or prevent them from spreading, it would prevent the bacteria from responding adequately to some antibiotic treatments. In this way, a substance blocking the SOS response could prolong the life of antibiotics, or allow the use of less powerful antibiotics to treat bacterial diseases.

References:

1: Žgur-Bertok D (2013) DNA Damage Repair and Bacterial Pathogens. PLoS Pathog 9(11): e1003711. doi:10.1371/journal.ppat.1003711

2: Edelweiss E, Balandin TG et al Barnase as a New Therapeutic Agent Triggering Apoptosis in Human Cancer Cells PLoS One. 2008 Jun 18;3(6):e2434.

S.E. Gould About the Author: A biochemist with a love of microbiology, the Lab Rat enjoys exploring, reading about and writing about bacteria. Having finally managed to tear herself away from university, she now works for a small company in Cambridge where she turns data into manageable words and awesome graphs. Follow on Twitter @labratting.

The views expressed are those of the author and are not necessarily those of Scientific American.





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