Ultraviolet Radiation Damage and Repair

Ultraviolet radiation is part of the electromagnetic spectrum, but with shorter, higher energy wavelengths than visible light. Prolonged exposure can be lethal to cells because when DNA absorbs UV radiation at 254 nm, the energy is used to form new covalent bonds between adjacent pyrimidines: cytosine-cytosine, cytosine-thymine, or thymine-thymine. Collectively, these are known as pyrimidine dimers, with thymine dimers being the most common. These dimers distort the DNA molecule and interfere with DNA replication and transcription (Fig. 10.18).

Many bacteria have mechanisms to repair such DNA damage. Escherichia coli performs light repair,
or photoreactivation, in which the repair enzyme, DNA photolyase, is activated by visible light (300-500 nm) and simply monomerizes the dimer by reversing the original reaction.

appropriate complementary nucleotides in a 5' to 3' direction to make the molecule double-stranded again. Finally, DNA ligase closes the gap between the last nucleotide of the new segment and the first nucleotide of the old DNA, and the repair is complete. Both mechanisms are capable of repairing a small amount of damage, but long and/or intense exposures to UV produce more damage than the cell can repair, making UV radiation lethal.

A second E. coli repair mechanism, excision repair, or dark repair, involves a number of enzymes (Fig. 10.19). The thymine dimer distorts the sugar-phosphate backbone of the strand. This is detected by UvrABC endonuclease (also known as ABC exinuclease) that breaks two bonds, one eight nucleotides in the 5' direction from the dimer, and the other four nucleotides in the 3' direction. A helicase (UvrD, also known as helicase II) removes the 14-nucleotide fragment (including the dimer), leaving 2.5'~ single-stranded DNA. DNA polymerase I inserts the appropriate complementary nucleotides in a 5' to 3' direction to make the molecule double-stranded again. Finally, DNA ligase closes the gap between the last nucleotide of the new segment and the first nucleotide of the old DNA, and the repair is complete. Both mechanisms are capable of repairing a small amount of damage, but long and/or intense exposures to UV produce more damage than the cell can repair, making UV radiation lethal.