SOS response: Difference between revisions

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InThe [[geneticsSOS response]] theis a postreplication [[SOSDNA responserepair]] issystem athat allows [[DNA replication]] repairto systembypass involvinglesions or errors in the [[DNA]]. The SOS uses the [[RecA]] protein. The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the [[LexA]] repressor thereby inducing the response. It is an error prone repair system.

==Mechanism==

During normal growth, the SOS genes are negatively regulated by the LexA repressor protein. Under normal conditions, LexA binds to a 20-bp consensus sequence (the SOS box) in the operator region of those genes . Some of these SOS genes are expressed at certain levels even in the repressed state, according to the affinity of LexA to 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. The activated form of RecA acts as a coprotease in the autocatalytic digestion of the LexA repressor, whose active form is as a dimer . Once the pool of LexA decreases, repression of the SOS genes goes down according to the LexA affinity to the SOS boxes. Operators that bind LexA relatively weakly are the first to be fully expressed. In this way LexA can sequentially activate different mechanisms of repair .

Genes having a weak LexA 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 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) is induced. SulA stops cell division, 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.

Once the pool of LexA decreases, repression of the SOS genes goes down according to the LexA affinity to the SOS boxes. Operators that bind LexA relatively weakly are the first to be fully expressed. In this way LexA can sequentially activate different mechanisms of repair. Genes having a weak LexA 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.

The SOS response was discovered and named by Miroslav Radman in 1974 (Radman, M. 1974. Phenomenology of an inducible mutagenic DNA repair pathway in Escherichia coli: SOS repair hypothesis, p. 128-142. In L. Prokash, F. Sherman, M. Miller, C. Lawrence, and H. W. Tabor (ed.), Molecular and environmental aspects of mutagenesis. Charles C Thomas Publisher, Springfield, Ill.). He is now Professor at the Faculté de Médecine - Necker, Université Paris V, Paris, France.

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) is induced. SulA stops cell division, 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.

==Discovery==

The SOS response was discovered and named by [[Miroslav Radman]] in 1974 (Radman, M. 1974. Phenomenology of an inducible mutagenic DNA repair pathway in Escherichia coli: SOS repair hypothesis, p. 128-142. In L. Prokash, F. Sherman, M. Miller, C. Lawrence, and H. W. Tabor (ed.), Molecular and environmental aspects of mutagenesis. Charles C Thomas Publisher, Springfield, Ill.). He is now Professor at the Faculté de Médecine - Necker, Université Paris V, Paris, France.

[[Category:DNA repair]]