How Is Uv Light Damage Repaired In Bacteria

LETHAL EFFECTS OF UV Radiations

UV calorie-free has a short wavelength (~10 to 400 nm). UV has a lethal effect on nearly organisms primarily because of its ability to cause the formation of thymine dimers in DNA. Thymine dimers are 2 side by side thymine bases that are abnormally linked together by covalent bonds. This dimerization inhibits DNA replication, which may lead to death of the organism.

Dimers form bumps in the Dna and disrupt the hydrogen bonding between bases on the complementary strands.

Since UV low-cal exerts a lethal result on bacteria information technology can be used to sterilize various objects such equally benches, surfaces of foods, utensils, etc. Because UV low-cal has very little penetrating power it is simply used for sterilization of surfaces.

Because mutations such as thymine dimers are potentially life threatening, cells accept a number of systems for finding and repairing damaged DNA. There are two main mechanisms more often than not used for repair of UV damaged DNA. The first mechanism is called photoreactivation (calorie-free repair) and the second is generally termed excision repair. As excision repair takes identify in the absence of light, information technology is likewise sometimes chosen dark reactivation.

Photoreactivation (light repair): The photoreactivation repair enzyme (PRE) is activated by visible light (400-750 nm). PRE uses blue light to break covalent bonds between thymine bases, allowing the hydrogen bonds to naturally reform.
Excision repair (nighttime reactivation): This repair process involves several enzymes:

a) An endonuclease called UvrABC¹ breaks the sugar phosphate backbone of the DNA strand nearly the dimer on each side.

b) The H-bonds between the base pairs are broken and a segment of DNA ~12 nucleotides long is excised.

c) DNA polymerase recognizes the 3'OH primer and fills in the missing bases.

d) DNA ligase seals the final saccharide-phosphate bail to repair the nicks.