Editing SOS response (section)

==Antibiotic resistance==
Research has shown that the SOS response system can lead to mutations which can lead to [[Antibiotic resistance|resistance]] to antibiotics.<ref name="Lee">{{cite journal | title=Inhibition of mutation and combating the evolution of antibiotic resistance |last1=Cirz | first1=RT |journal=PLOS Biology |date=June 2005 |volume=3 |issue=6 |page=e176 |doi=10.1371/journal.pbio.0030176 |pmid=15869329 |last2=Chin |first2=JK |last3=Andes |first3=DR |last4=De Crécy-Lagard |first4=V |last5=Craig |first5=WA |last6=Romesberg |first6=FE |pmc=1088971 |doi-access=free}} {{open access}}</ref> The increased rate of mutation during the SOS response is caused by three low-fidelity [[DNA polymerase]]s: [[Pol II]], [[Pol IV]] and [[Pol V]].<ref>{{cite journal |title=Mutations for Worse or Better: Low Fidelity DNA Synthesis by SOS DNA Polymerase V is a Tightly-Regulated Double-Edged Sword |last1=Jaszczur |first1=M |journal=Biochemistry |date=April 2016 |volume=55 |issue=16 |pages=2309–18 | doi=10.1021/acs.biochem.6b00117 | pmid=27043933 |last2=Bertram |first2=JG |last3=Robinson |first3=A |last4=van Oijen |first4=AM |last5=Woodgate |first5=R |last6=Cox |first6=MM |last7=Goodman |first7=MF |pmc=4846499}}</ref><ref name="Lee"/> Researchers are now targeting these proteins with the aim of creating drugs that prevent SOS repair. By doing so, the time needed for pathogenic bacteria to evolve antibiotic resistance could be extended, thus improving the long term viability of some antibiotic drugs.<ref>{{cite journal |title=A molecular target for suppression of the evolution of antibiotic resistance: Inhibition of the ''Escherichia coli'' RecA Protein by N6-(1-Naphthyl)-ADP |last1=Lee |first1=AM |last2=Ross |first2=CT |last3=Zeng |first3=BB |last4=Singleton |first4=SF |journal=Journal of Medicinal Chemistry |date=July 2005 |volume=48 |issue=17 |pages=5408–5411 |doi=10.1021/jm050113z |pmid=16107138}}</ref>

As well as genetic resistance the SOS response can also promote phenotypic resistance. Here, the genome is preserved whilst other non-genetic factors are altered to enable the bacteria to survive. The SOS dependent [[TisB-IstR toxin-antitoxin system|tisB-istR]] [[toxin-antitoxin system]] has, for example, been linked to DNA damage-dependent [[Persister cells|persister cell]] induction.<ref>{{cite journal |title=Ciprofloxacin Causes Persister Formation by Inducing the TisB toxin in ''Escherichia coli'' |last1=Dörr |first1=T |journal=PLOS Biology |date=February 2010 |volume=8 |issue=2 |pages=e1000317 |pmc=2826370 |doi=10.1371/journal.pbio.1000317 |pmid=20186264 |last2=Vulić |first2=M |last3=Lewis |first3=K |doi-access=free}}</ref>