How does the cell prevent mutation?

How does the cell prevent mutation?

Unintended chemical changes such as the formation of thymine dimer, depurination, and deanimation affect DNA replication in a bad way, causing the substitution of one nucleotide pair for another and the deletion of nucleotide pairs in the daughter DNA strand. Cells need to prevent those mutations from occurring, but how?

There are two cases, depending on which the cell determines what kind of measure to take. The first case is when only nucleotides on one strand are damaged. In this case, they can be repaired using the information present in the complementary strand in two different ways. The first one is to cleave the covalent bonds that join the damaged nucleotides to the rest of the DNA strand by nucleases or other enzymes(the type of enzyme used in this reaction changes depending on the situation), then fill in the gap by making a complementary copy of the information stored in the undamaged strand using repair DNA polymerases, and lastly seal the nick by DNA ligase. Given that most DNA damage creates structures that are never encountered in an undamaged DNA strand, it is easy for these enzymes involved in these steps to differentiate between the good strands and the bad. The second way is called mismatch repair. The system restores the correct sequence, removing a portion of the DNA strand containing the error and resynthesizing the missing DNA. This way is effective only in the case of newly synthesized DNA.

(For your information)

An inherited predisposition to certain cancers is caused by mutations in genes that encode mismatch repair proteins. Humans inherit two copies of these genes from each parent. If one inherits two damaged mismatch repair genes, they cannot prevent mutations by mismatch repair and thus have a higher possibility to get cancer. Humans who inherit one damaged mismatch repair gene is unaffected until another mismatch repair gene is mutated in a somatic cell. 

The second case is that both strands are damaged. Cells adopt two ways against this case: nonhomologous end joining and homologous recombination. Nonhomologous end joining is carried out by nucleases which clean the broken ends and by DNA ligase which rejoins them. However, this mechanism have a weakness in that nucleotides are often lost in the phase of broken end cleaning. Homologous recombination mostly occurs shortly after a cell’s DNA has been replicated before cell division. A nuclease digests 5’ ends of broken strands, and then with the help of specialized enzymes, one of the broken 3’ ends invades the unbroken homologous DNA duplex, and DNA ligation follows after a repair DNA polymerase resynthesizing DNA.