Mutation Repair Flashcards
(20 cards)
Mismatch Repair Can Fix
Incorrect Base Pair
Nucleotide Excision Repair Can Fix
Altered Base, deletion or insertion, linked pyrimidines (UV radiation), cross-linked strands (STRUCTURAL DISTORTIONS)
Homologous Recombination Can Fix
single or double stranded breaks caused by ionization or chemotherapy
Nonhomologous End Joining Can Fix
single or double stranded breaks caused by ionization or chemotherapy
Translesion DNA synthesis Can Fix
cross-linked strands, linked pyrimidines
Mutation
heritable change in the sequence of DNA (change in genotype) - Watson crick pair changed to another normal W-C pair, not recognized as a mistake
Damage
altered pairing (not W-C pair) that can still be recognized as a mistake (can turn into a mutation if not recognized)
Mismatch Repair Mechanism
Corrects incorrect base pairings 1. MutH recognizes daughter strand (non-methylated) in prokaryotes (time sensitve) 2. MutS finds the mismatch 3. MutL binds S and H together 4. Mut H nicks daughter strand 5. helicase, exonuclease, DNA Pol and ligase do their jobs to resynthesize area
Direct-Acting Mutagens
covalently modify DNA bases
Indirect-Acting Mutagens
are water soluble and inert until activated by liver cytochrome P-450
Nucleotide Excision Repair Mechanism
repairs environmentally-induced DNA damage, not time sensitive (can happen anytime) 1. distortion recognized in DNA by a protein dimer 2. Helicase and Stabilizers are recruited 3. incisions are made at 3’ and 5’ sides of distortion 4. Dna pol fills gap and ligase seals it
Homologous Recombination Mechanism
repairs double stranded breaks (most lethal), this repair mechanism is the accurate way to join breaks (no lost info), uses strand invasion of homologous DNA strand from sister chromatid to resynthesize chromosomal DNA (MUST happen in S or G2 phases of cell cylce)
Holliday Junctions
crossover points in homologous recombination between sister chromatids
Nonhomologous End Joining Mechanism
error-prone rescue replication of double stranded breaks, predominant pathway, no specificity, CAUSES PROBLEMS! 1. DNA is unwound until a complementary sequence is found between the two broken double helices 2. once that is found they are joined together
Reciprocal Translocation
problem with nonhomologous end-joining where ends of two different chromosome are switched with each other
Inversion
problem with nonhomologous end-joining where the center of a chromosome is rejoined backwards from original orientation
Translesion DNA synthesis Mechanism
if DNA polymerases encounters conformational change because of damage it will dissociate and TLS DNA pol will take over. TLS DNA pol has reduced fidelity and can accomodate altered pairings and continue synthesis. error prone and low processivity - will dissociate after a few bases and DNA pol will take back over
Ames Test
test for mutagenic capabilities of compounds
How does the Ames Test work?
use a His- bacteria (cannot replicate) and put mutagen in to see if any collonies grow (would have to be mutated). Can also add liver extract to see if mutagen is indirect or direct (will grow if indirect w/ liver extract)
What are limitations of the Ames Test?
Only detects mutations to the His gene, says whethere a compound is mutagenic, not carcinogenic