p53

tumor-suppressor gene 

arrest of cells with damaged DNA

TLS Online TPP Program

#Id: 3371

#Unit 3. Fundamental Processes

Structural studies show that the active site of DNA Pol h is better at accommodating a thymine dimer than is the active site of another translesion DNA polymerase (DNA Pol k

TLS Online TPP Program

#Id: 3374

#Unit 3. Fundamental Processes

Translesion synthesis replicates across the DNA lesion, but the lesion remains in the genome until a DNA repair pathway can subsequently correct the damage.

TLS Online TPP Program

#Id: 3393

#Unit 3. Fundamental Processes

Because of its high error rate, translesion synthesis (like NHEJ) can be considered a system of last resort. It enables the cell to survive what might otherwise be a catastrophic block to replication, but the price that is paid is a higher level of mut

TLS Online TPP Program

#Id: 3396

#Unit 3. Fundamental Processes

The genes encoding the translesion polymerases are expressed as part of a pathway known as the SOS response. 

TLS Online TPP Program

#Id: 3397

#Unit 3. Fundamental Processes

Damage leads to the proteolytic destruction of a transcriptional repressor (the LexA repressor) that controls expression of genes involved in the SOS response, including those for DinB, UmuC, and UmuD, the inactive precursor for UmuD0.

TLS Online TPP Program

#Id: 3400

#Unit 3. Fundamental Processes

Cleavage of both LexA and UmuD is stimulated by a protein called RecA, which is activated by single-stranded DNA resulting from DNA damage.