Editing SOS response (section)

==Mechanism==
During normal growth, the SOS genes are under the repressor of the [[LexA]] protein. Under normal conditions, LexA binds to a  consensus sequence (the [[SOS box]]) in the operator region of the SOS regulon genes. Some of these genes are expressed at certain levels even in the repressed state, according to the affinity of LexA for their SOS box. Activation of the SOS genes occurs after DNA damage by the accumulation of single stranded (ssDNA) regions generated at replication forks, where [[DNA polymerase]] is blocked. RecA forms a filament around these ssDNA regions in an ATP-dependent fashion, and becomes activated.<ref name=":30447030">{{cite journal |title=The SOS system: A complex and tightly regulated response to DNA damage |journal=Environmental and Molecular Mutagenesis |date=May 2019 |volume=60 |issue=4 |pages=368–384 |doi=10.1002/em.22267 |pmc=6590174 |pmid=30447030 |last1=Maslowska |first1=K. H. |last2=Makiela-Dzbenska |first2=K. |last3=Fijalkowska |first3=I. J. |bibcode=2019EnvMM..60..368M}}</ref> The activated form of RecA interacts with the LexA repressor to facilitate the LexA repressor's self-cleavage from the operator.<ref name=":30447030" /><ref>{{cite book |last1=Lehninger |first1=Albert L. |last2=Nelson |first2=David Lee |last3=Cox |first3=Michael M. |title=Lehninger principles of biochemistry |date=2005 |publisher=W.H. Freeman |location=New York |isbn=978-0-7167-4339-2 |edition=4th |page=1098 |oclc=55476414}}</ref>

Once the pool of LexA decreases, repression of the SOS genes goes down according to the level of LexA affinity for the SOS boxes.<ref name=":30447030" /> Operators that bind LexA weakly are the first to be fully expressed. In this way LexA can sequentially activate different mechanisms of repair. Genes having a weak SOS box (such as ''lexA'', ''recA'', ''uvrA'', ''uvrB'', and ''uvrD'') are fully induced in response to even weak SOS-inducing treatments. Thus the first SOS repair mechanism to be induced is [[nucleotide excision repair]] (NER), whose aim is to fix DNA damage without commitment to a full-fledged SOS response. If, however, NER does not suffice to fix the damage, the LexA concentration is further reduced, so the expression of genes with stronger LexA boxes (such as ''sulA'', ''umuD'', ''umuC'' – these are expressed late) is induced.<ref name=":30447030" /> SulA stops [[cell division]]<ref name=":30447030" /> by binding to [[FtsZ]], the initiating protein in this process. This causes [[filamentation]], and the induction of UmuDC-dependent mutagenic repair. As a result of these properties, some genes may be partially induced in response to even endogenous levels of DNA damage, while other genes appear to be induced only when high or persistent DNA damage is present in the cell.