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29 Cards in this Set
- Front
- Back
Mismatch Repair |
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Endonuclease |
(nickase) cleaves DNA bonds within DNA molecules |
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Exonuclease |
cleaves thenucleotides at the end of aDNA molecule, requires free3’ or 5’ –OH, works with ahelicase |
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Mut H |
- endonuclease that creates a nick on the new strand of DNA in MR - binds the nearest GATCmethylated sites andcuts only non-methylated DNA |
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Intercalating agents |
Cause the addition of base pairs byslipping between the bases in the template strand |
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Uvr |
genes for nucleotide excisionrepair - loss leads to UV sensitivity |
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Rad |
genes for double-strand breakrepair - loss leads to radiationsensitivity |
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Mut |
genes for mismatch repair -loss results in high mutation rate |
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OxoG |
can be mispaired to A |
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O6-methyl G |
can be mispaired to T (BER) |
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Base-Excision Repair |
one of two types of excision: acts on a single damaged nucleotide (BER and DR) 1. DNA glycolysase recognizes and removes damaged base. 2 AP endonuclease recogs abasic site. 3. replacement via polymerase and ligase |
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Hydrolytic Reactions |
-deamination of cytosine to uracil -depurination leaves an abasic site |
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DNA Glycolisase |
flips the damaged base to expose the damaged site that will be cleaved and removes it |
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Damage Reversal (DR) |
-mostly in bacteria only -degrades protein after process (enzyme is methylated and site is demethylated) -uses methyltransferase to transfer methyl group from one substrate. -focus on O6-methylG transferase -very efficient yet consuming because methylated enzyme is degraded (sacrifice an entire protein) |
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Trans-letion Synthesis (TLS) |
- allows damage, not repair -flexible but causes mutation - Uniquitination triggers the switch to a trans-lesionpolymerase in mammalian cells - In E. Coli, Pol IV and V come in a and replace the stalled polymerase at the fork and incorporate random bases. |
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RPA |
(Replication protein A) damage sensor: single stranded binding protein that binds DNA ahead of the polymerase at the rep fork--->>> recruits ATR which phosphorylates H2AX keeps the DNA unwound for repair/replication |
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MRN |
damage sensor: recognizes DNA double strand breaks--->>> Recruits ATM which phosphorylates H2AX |
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Swr1 and Ino80 |
-chromatin remodelers -promote strand invasion byproviding access to the donor sequence |
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NHEJ |
-error prone, fast, G1 -doesnt require homology -rejoines 2 ends |
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Single Strand Annealing (SSA) |
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Alt-EJ |
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MRN-Ctip |
endonuclease that initiates resection in HR works with wrn helicase |
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Endonucleases that extends resection |
Dna2 (endonuclease) blm (3'-5' helicase) exo1 (exonuclease) |
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Werner syndrome |
Cancer predisposition- Telomeric instability- Premature aging due to Wrn mutation |
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RecA/Rad51 |
binds to ssDNA, replaces RPA, forms a filament around ssDNA and probes for homology (needs more than 15bp), and drives strand invasion |
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Brca2 |
-subs RPA with rad51 -mutation responsible for breast cancer |
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RuvAB |
promotes Holliday Junction migration in bacteria only RUV A recognizes holliday junctions Ruv B helicase promotes movement Ruv C resolves Holliday Junctions by cleaving acrossthe Junction |
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Blm helicase & top3 isomerase |
requires for HJ dissolution helicase can revert recombination intermediates by displacing rad51 topoisomerase activity counteracts positivesupercoiling during dissolution by creating breaks in the DNA to resolve topological issues |
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CRISPR/Cas9 |
-used as a research tool -Cas9 can be directed to ANY target sequence toinduce DSBs and improve gene targeting |