Light dependent repair uv light creates a thymine

Light dependent repair
- UV light creates a thymine dimer
- DNA photolyase binds to dimer
- Photolyase is activated by absorption of blue light
- Cross links between dimer are cleaved, photolyase released
- Only in PROKARYOTES
Excision repair
- Base excision repair
- Nucleotide excision repair
Basic features are similar
- DNA repair endonuclease or endonuclease-containing complex recognizes, binds and
excises damaged base/bases
- DNA polymerase fills in the gap, using the undamaged complementary strand of DNA as
a template
- DNA ligase seals the break left by DNA polymerase
Nucleotide excision repair (NER)
- In prokaryotes, complex of UvrA, B, C proteins results in detection and removal of
thymine dimer caused by UV light, followed by polymerase I fill in and ligation
- In humans, NER also acts to remove thymine dimers and other bulky forms of DNA
damage
- This one removes big lesions while base excision repair removes smaller ones
- Mutation of NER genes in humans causes XERODERMA PGMENTOSUM
- BOTH PROKARYOTES AND EUKARYOTES
DNA Mismatch repair in E coli
- Aids in removal of incorrect insertions and deletions
- MutS recognizes mismatches and binds to initiate repair process
- MutH and MutL join complex
- MutH cleaves the unmethylated strand at hemi-methylated GATC sequences on either
side of mismatch
- MutH compares old and new strands based on methylation status of “A” in the sequence
5’ GATC 3’
- Excision requires MutS, MutL, (MutU – DNA helicase) and an exonuclease
- DNA polymerase III fills in gap, DNA ligase seals nick

- Defencts in human mismatch repair result in mutation accumulation and are directly
connected to hereditary colorectal cancer
- BOTH PROKARYOTES AND EUKARYOTES
Post-replication Recombination repair
- Involves pairing and strand exchanges between DNA duplexes
- Provides a mechanism for T:T to be bypassed so that the replication can continue
- T:T may be removed by another mechanism (NER or mismatch repair)
- Recombination also repairs double stranded breaks in chromosomes most often through
interactions with undamaged, newly replicated chromosomes
- BOTH PROKARYOTES AND EUKARYOTES
Error prone repair – SOS response
- If DNA is heavily damaged, SOS response (involving DNA recombination, repair and
replication proteins) is activated
- Much of DNA damage might be fixed by NER, BER and normal DNA replication processes
- However DNA polymerase III cannot replicate heavily damaged DNA, thus error prone
DNA polymerase IV and V are recruited to copy damaged DNA, but they’re inaccurate –
get error prone DNA synthesis
- This error prone system aids in DNA replication but increases frequency of replication
errors
- Error prone replication is a mechanism of LAST RESORT
- OCCURS IN PROKARYOTES AND EUKARYOTES