BIO 3170 Lecture Notes - Lecture 5: Dna Mismatch Repair, Dna Replication, Dna Repair

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20 Dec 2018

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Objective: describe various steps of strand-directed mismatch repair. Name various factors contributing to high delity of dna replication. Objective: name 2 spontaneous modi cations that can affect dna bases. Objective: describe the steps of base excision repair & nucleotide excision repair. Objective: name & describe 2 mechanisms responsible for repair of double stranded breaks. Homologous recombination exchange of genetic info bwth a pair of identical14 similar dnaseq relies on base pairing interactions. Steps binaon precise repair of dsdna breaks overcome stalledreplication fork producegenetic variation during meiosis crossing over. Objective: name & describe the steps of homologous recombination. Entraasinodn the dna in the intact helixbe freedmaking its nucleotides available strand invasion. Objective: explain the role of reca (or rad51) during recombination pairing ssdnasegment w complementary strand in a diff dnahelix requires that for pairing. Branch migration point of strand exchange can move thru branch migration unpaired ss displace original paired strand who is the total paired bases can occur.

Related Questions

What are the advantages of recombination? What are the disadvantages? Under what kinds of ecological conditions (stable environment, high predation rates, exposure to rapidly evolving parasites, etc.) would you expect to favor one, or the other?

Suppose you found a region of a genome in a vertebrate that was quite large (say, 10 million base pairs) that had an extremely low recombination rate. Suggest a reason why it might be advantageous to not recombine the genes in that genomic region.

How do prokaryotes distinguish the newly synthesized strand from the old template strand? Why donât eukaryotes use the same mechanism?

What is methylation used for in prokaryotes? In eukaryotes?

What happens if mismatch repair occurs shortly after replication? How does it know which mismatched, normal base is incorrect? What happens if mismatch repair occurs long after replication has occurred?

Why does uracil DNA glycosylase have so an easier task to perform than thymine DNA glycosylase?

Describe the steps that occur following uracil DNA glycosylase activity. What needs to happen; what enzymes are involved?

What do x-rays do to DNA? What does UV radiation do? What do microwaves do?

Is there a safe minimum dose of radiation?

Why is telomerase turned off in human somatic cells? Is it turned off in mouse somatic cells? Would you expect it to be turned off in elephants? Would you expect elephants to have high cancer rates compared to mice?

Where is telomerase necessary? Is it on the leading, or lagging strand, or both? Why donât bacteria need telomerase?

Why is microsatellite instability used by physicians to measure problems with mismatch repair?

Identify and briefly describe three of the processes by which deamination of DNA-cytosine residues by AID could lead to mutagenesis.

Fill in the blanks.

The most likely pathway would involve deamination of________1_________ to _______2________ , with the U templating_____3_________ on the next round of synthesis. Another possibility is for_______4________ to create an abasic site after removing ________5_________created by deamination, with________6__________ then being inserted opposite that site during the________7_______ , before the ________8_______can be completed. A third possibility would be repair of the GâU mismatch by _________9__________ or _______10_________, giving an__________11______ pair that would replicate to give_________12___________ .

Word Bank: (each word can only be used once)

any base	next round of replication	U	GâC	AâU	UNG	NER
mismatch repair	repair process	G	A	T	GâU	AâT

Benzo[a]pyrene, the cancer-causing agent in cigarette smoke, is a powerful mutagen. Benzo[a]pyrene itself is relatively harmless, but it is metabolized in the liver to produce active molecules that react covalently with DNA. In an experiment, benzo[a]pyrene is incubated with a mixture of liver enzymes to form its genotoxic metabolites. These metabolites are added to E. coli cells that have a mutation in a gene encoding an enzyme of the serine-synthesizing pathway (i.e., the cells are serine auxotrophs, requiring serine for growth). When the treated cells are grown on serine-containing medium, the results show that the benzo[a]pyrene metabolites kill cells in a dose-dependent manner. When treated and untreated serine-auxotrophic cells are plated separately on serine-free media, the cells treated with benzo[a]pyrene metabolites show a 10- to 100-fold increase in survivors compared with untreated cells. Explain these results.Compare and contrast mismatch repair in E. coli and eukaryotes.

List two reasons translesion sysnthesis tends to be mutagenic.

Describe, in detail, nucleotide excision repair. Include especially ways the damage can be recognized.

BIO 3170 Lecture Notes - Lecture 5: Dna Mismatch Repair, Dna Replication, Dna Repair

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