Light dependent repair UV light creates a thymine dimer DNA photolyase binds to

Light dependent repair uv light creates a thymine

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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
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- 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
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