Sos repair

SOS response was discovered by Miroslav Radman. It's a part of DNA repair system- synthesizes enzymes required for DNA repair. Cellular response to UV damage.

1. DNA REPAIR -SOS REPAIR MECHANISM

2. Safeguarding the genome: I f DNA is the master copy of instructions for an organism, then it is important not to make mistakes when copying the DNA to pass on to new cells. All DNA suffers damage over time, from exposure to ultraviolet and other radiation, from various chemicals in the environment, point mutations… Maintaining the integrity of the cell's "blueprint" is of vital importance and this is reflected in the numerous mechanisms that exist to repair mistakes and damage in DNA DNA damage: DNA damage is a change in the basic structure of DNA that is not itself replicated when the DNA is replicated What causes damage to DNA? a. Radiation (e.g., UV rays in sunlight and in tanning booths, or ionizing radiation)​ b. Exposure to damaging chemicals, such as nitrosamines or polycyclic aromatic hydrocarbons c. Chemical reactions within the cell (such as the deamination of cytosine to give uracil, or the methylation of guanine to produce methylguanine).

3. DNA REPAIR: A collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. DNA repair process is constantly active as it responds to damage in the DNA structure. Different DNA repair pathways includes—base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR) and non-homologous end joining (NHEJ)—are active throughout different stages of the cell cycle, allowing the cells to repair the DNA damage.

4. SOS response The SOS response was discovered and named by  Miroslav Radman  in 1975. A global response to DNA damage in which the  cell cycle  is arrested and DNA repair  and  mutagenesis  is induced. It’s a part of DNA repair system; synthesizes DNA repair enzymes. Named for standard SOS distress signals ( stands for “ Save Our Soul ” ), the term “SOS repair” refers to a cellular response to UV damage D amage done by UV rays : two adjacent pyrimidine bases in the DNA will be cross-linked to form cyclobutane pyrimidine dimers or CPDs UV exposure can also lead to the formation of another type of lesion, known as a (6-4) photoproduct or 6-4PP

5. Elements: An SOS system is composed of the following components Repressor gene : encoded by the “ LexA ” gene - causes the inactivation of inducer proteins. The repressor binds to the operator and causes inactivation or repression of the SOS system. Regulator gene : encoded by the “ RecA ” gene - to activate the repressed SOS system by inhibiting the binding of LexA to the SOS operator. Inducer/structural genes : They are encoded by SOS-box genes that can activate the inducer proteins relative to the type of DNA damage. -Includes- uvrA , umuC , umuD …

6. SOS proteins Encoded by Functions Regulatory protein RecA gene It functions as regulator of SOS system Repressor protein LexA gene It functions as inhibitor of SOS system Inducer proteins uvrA gene Repairs short patch nucleotide damage, cross-links and long patch nucleotide damage umuC gene It functions to bypass the lesion site of DNA and leads to mutagenesis umuD gene It functions to bypass the lesion site of DNA and leads to mutagenesis

7. SOS RESPONSE In  normal DNA , a bacterial cell does not need DNA repair genes to be activated. Thus, there should be some controller that must control the expression of such genes. LexA acts as a repressor protein by binding to a 20-bp consensus sequence , the SOS box. The binding will repress the activity of SOS genes. But in damaged DNA , the inactivation of LexA repressor becomes necessary to induce the expression of SOS genes. RecA acts as an activator of SOS genes in the SOS system, which causes proteolysis of the repressor protein and allows the SOS genes expression into different DNA repairing inducer proteins.

8. Mechanism of SOS Repair The mechanism of SOS repair is a complex cellular process mediated by the organism itself. It includes the following steps: In case of excessive DNA damage, stress conditions etc., a cell responds by activating signal or  RecA  protein. It floats in the vicinity of the cell in search of any damage in the DNA. A RecA protein specifically binds to the single stranded DNA. On binding with the single stranded DNA fragments, RecA forms a  filament-like  structure around the DNA. Then, a LexA repressor comes in contact with the nucleoprotein filament assembled by the RecA protein. When RecA interacts with the repressor protein, it gets converted to  RecA protease . The formation of RecA protease causes autocatalytic  proteolysis of LexA  repressor protein. Thus, a LexA protein cannot bind with the SOS operator. Inactivation of LexA protein activates the inducer proteins that repair the DNA damage but alters the DNA sequence. After DNA repair, the RecA protein loses its efficiency to cause proteolysis, and the LexA protein will again bind to the SOS operator or  switch off  the SOS system.

9. Nucleotide Excision Repair (NER) : After UV irradiation, the amount of Lex A repressor decreases nearly 10 -fold in a few minutes. The SOS genes, however, are not all induced at the same time and to the same level. The first genes to be induced are endonuclease uvr A, uvr B, and u vr C, that catalyze nucleotide excision repair (NER). These endonuclease enzymes excises or cleaves the damaged nucleotides from ds DNA. The excised region undergoes polymerization and then ligation.

10. Translesion DNA synthesis: T ranslesion DNA synthesis (TLS) is  the process by which cells copy DNA containing unrepaired damage that blocks progression of the replication fork . TLS is a DNA damage tolerance process that allows the DNA replication machinery to replicate past DNA lesions such as  thymine dimers . Occurs when other repairs are not efficient. When NER doesn’t fix the damage umu C and umu D genes synthesizes DNA polymerase V (   that has larger active sites which can facilitate the insertion of bases opposite damaged nucleotides ) DNA polymerase V replaces the normal replicative polymerase ( i.e DNA polymerase III) and continues the replication across the lesion and prevents cell from having unreplicated chromosome at the cost of some point mutations.

11. REFERENCES: https://en.wikipedia.org/wiki/SOS_response https://biologyreader.com/sos-repair.html Biology libre texts.html