The seminar discussed DNA damage and repair mechanisms. DNA can be damaged through spontaneous chemical bond cleavage, environmental agents like UV radiation, and genotoxic chemicals. A common type of UV damage is thymine dimers, which interfere with DNA replication and transcription. Nucleotide excision repair is a system that fixes chemically modified bases and adducts using 30 proteins that slide along DNA. Diseases like xeroderma pigmentosum are caused by an inability to repair damaged DNA, leading to increased skin cancer susceptibility.

1. SEMINAR PRESENTED BY
RODU JAMES LS
1ST SEMESTER
MSc BIOTECHNOLOGY

2. Damage to DNA is unavoidable
The Damage is caused by :-
•Spontaneous cleavage of chemical bonds in DNA.
•Environmental agents such as ultraviolet & ionizing
radiation.
•Reaction with genotoxic chemicals.
•Mutation

3. THYMINE DIMER
1. A common type of damage caused by UV light.
2.These Dimers interfere with both replication and
transcription of DNA.

4. EFFECT OF UV RADIATION
 Radiation with a wavelength of about 280nm is
strongly absorbed by the bases.
 One consequence of which is the photochemical
fusion of two adjacent Thymine.
 The thymine dimer comprise of a cyclobutane ring.
 This ring is generated by links between carbon
atoms 5 & 6 of adjacent thymines.

5. Diagram of
thymine dimer

6. NUCLEOTIDE EXCISION
REPAIR
 This DNA repair system fix DNA region containing
chemically modified bases, chemical adducts.
 The key here is the ability of certain proteins to slide
along the surface of dsDNA molecule.
 Some 30 proteins are involved in this repair process.

7. NUCLEOTIDE
EXCISION REPAIR


8. Disease caused due to the absence of NER.
Xeroderma Pigmentosum
 Xeroderma pigmentosum is an autosomal recessive
genetic disorder.
 People suffering from this disorder are often called
“children of the night’’.
 They lack the ability to repair damaged DNA.
 Cancer susceptibility – Skin carcinomas
-- Melanomas
 Symptoms - Skin & eye photosensitivity.

9. References
 Molecular Biology of Gene ; Watson et al
 Cell & Molecular Biology ; Lodish et al
 Wikipedia.