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Lecture 9

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Western University
Biology 1001A

Lecture 9:  Clicker Question: When does crossing over occur between homologous chromosomes   Prophase 1 of meiosis  List of mechanisms to generate genomic diversity   Transposition (Mobile elements)  Copy number variation (Ex. slippage)  Ability of repair damage (Ex. Dimers) and DNA polymerase  Repairing double stranded breaks create copy number variations in a genome  Mutations  physical mutations caused by radiation, by environmental factors  Tautomeric shifts happen spontaneously   T-A and C-G are normal pairs  T-G and C-A are tautomeric shifts  Clicker Question: Why is the wrong tautomeric form of thymine not removed by mismatch repair   Mismatch pair doesn't break H bonds, it breaks the backbone -> A is wrong  DNA polymerase is not part of mismatch repair, DNA polymerase is used for proofreading -> C is wrong  If thymine switched to it's other tautomer it would still be matched with a G -> D is wrong  Therefore the answer is B since the pairings doesn't distort the helix  cannot be detected by mismatch repair, cannot be fixed  Some mutagens are tautomerically unstable base "analogues"   thymine and uracil the difference is only the methyl group  Thymine is just methyluracil  5-Bromouracil is a base analogue (looks like thymine) have time telling the difference from 5- bromouracil and thymine   got into the genome by mistake  5-Bromouracil is tautomerically unstable and is a mechanism for chemical mutagenesis   chemical can increase the mutation rate  DNA polymerase can't distinguish 5-Bromouracil from thymine since they are so similar  5-Bromouracil gets incorporated into your DNA during replication instead of thymine  Tautomeric shifts happen naturally  UV radiation causes thymine dimers that distort the helix   The ring structure of thymine absorbs the photon of ultraviolet light and rearranges the electrons in its ring structure  The helix is distorted because 2 thymine bases actually bond together (called a dimer)  Very difficult for polymerases to transcribe/replicate through a dimer, they stall at dimers (this can be lethal)   distort the DNA like crazy  in some organisms Polymerase relaxes some replication rules so any base is inserted in the damaged area which causes mutation  Dimer isn't the mutation, but rather the cell's attempt of staying alive by putting random bases down cause the mutation  Dimers can be repaired by photolyase or excision   Photolyase + white light (blue) undoes/break the dimer (solar powered)  want to try to fix it, in humans its easier for it to die than to cause mutations  Mammals (Ex. humans, dogs, horses, whales) don't have photolyase (Ex. Plants, bacteria etc. has it though)   how a group of organisms that can lose photolyase, (learn by the end of course)  Evolution doesn't always increase complexity  Humans use excision repair   Nuclease enzyme cuts out the damaged DNA at two points and the damaged section is removed  Repair synthesis by a DNA polymerase fills in the missing nucleotide
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