The SOS gene is involved in DNA repair in E. coli. It is activated in response to DNA damage and induces DNA repair and mutagenesis through the RecA and LexA proteins. RecA binds to single-stranded DNA and promotes self-cleavage of the LexA repressor, allowing expression of SOS genes involved in DNA repair pathways like nucleotide excision repair and error-prone repair. This response allows E. coli to repair its DNA but can also lead to increased mutagenesis.

1. SOS GENE ROLE IN E.COLI
1.WHAT IS SOS GENE?
2.WHAT ITS MECHANISM
3.WHAT ITS ROLE IN REPAIRING OF DNA
5.REFERENCES

2. WHAT IS SOS GENE?
•SOS gene is the gene which is role in cell
signalling,mutagenesis,more important in DNA
repairing.
•SOS gene basically called ‘SAVE OUR SOULS’ in
Dna repairing in E.COLI
•SOS gene have role in cell signalling,called
as’’sons of sevenless’’

3. Sos role in apoptosis
’

4. Sos response
• SOS response
• The SOS response is a global response to DNA damage in which the cell
cycle is
• arrested and DNA repair and mutagenesis are induced. The system involves
the
• RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by
singlestranded
• DNA, is involved in the inactivation of the LexA (repressor of SOS
• response genes) thereby inducing the response. It is an error-prone repair
system that
• is attributed to mutagenesis.

5. Sos mechanism
• During normal growth, the SOS genes are negatively regulated by LexA repressor protein
dimers. Under normal conditions, LexA
• binds to a 20-bp consensus sequence (the SOS box) in the operator region for those
genes. Some of these SOS 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. The activated
• form of RecA interacts with the LexA repressor to facilitate the LexA repressor's self-
cleavage from the opera.t[o3r]
• Once the pool of LexA decreases, repression of the SOS genes goes down according to
the level of LexA affinity for the SOS boxes.

6. Continue…………..
• 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 isn ucleotide excision repair
(NER), whose aim is to fix DNA damage without commitment to a
• full-fledged SOS response.
• cell.

7. Continue…………………….
• 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. SulA stops cell division 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.

8. Fig.

9. Role in genotoxicity
• In Escherichia coli, different classes of DNA-damaging agents can initiate the SOS
• response, as described above. Taking advantage of an operon fusion placing the lac
• operon (responsible for producing beta-galactosidase, a protein which degrades
• lactose) under the control of an SOS-related protein, a simple colorimetric assay for
• genotoxicity is possible. A lactose analog is added to the bacteria, which is then
• degraded by beta-galactosidase, thereby producing a colored compound which can
• be measured quantitatively through spectrophotometry. The degree of color
• development is an indirect measure of the beta-galactosidase produced, which itself
• is directly related to the amount of DNA damage.

10. References
• 1. Michel B (2005). "After 30 Years of Study, the Bacterial
• SOS Response Still Surprises Us" (https://www.ncbi.nlm.ni
• h.gov/pmc/articles/PMC1174825). PLoS Biology. 3 (7):
• e255. doi:10.1371/journal.pbio.0030255 (https://doi.org/1
• 0.1371%2Fjournal.pbio.0030255). PMC 1174825 (https://
• www.ncbi.nlm.nih.gov/pmc/articles/PMC1174825) .
• PMID 16000023 (https://www.ncbi.nlm.nih.gov/pubmed/16
• 000023).
• 2. Radman, M (1975). "Phenomenology of an inducible mutagenic DNA repair pathway in Escherichia coli: SOS repair
• pichulein hypothesis". Basic Life Sciences. 5A: 355–367. PMID 1103845 (https://www.ncbi.nlm.nih.gov/pubmed/110
• 3845).
• 3. Nelson, David L., and Michael M. Cox. Lehninger: Principles of Biochemistry 4th Edition. Newo Yrk: W.H. Freeman
• and Company, 2005. page 1098.
• 4. Little JW, Mount DW (May 1982). "The SOSR egulatory System of Escherichia coli".C ell. 29 (1): 11–22.
• doi:10.1016/0092-8674(82)90085-X (https://doi.org/10.1016%2F0092-8674%2882%2990085-X.)