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Chapter 16
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Fredrick Griffith – 1928 Studying Streptococcus pneumonia 2 strains – Rough (non- lethal) and Smooth (lethal) Through a series of experiments discovered transformation
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Oswald Avery – 1944 Used Griffith’s transformation data Wanted to see which substance transferred DNA, RNA, or Proteins Treated each of the three substances sequentially Treatment inactivated one type of molecule
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Alfred Hershey and Martha Chase – 1952 Were not convinced it was DNA Used a bacteriophage with radioactive labels Sulfur – protein Phosphorus – DNA Upon analysis found the DNA entered the bacteria
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Erwin Chargaff - 1950 Already knew composition of a nucleotide Sugar (deoxyribose/ribose, phosphate group, and a nitrogenous base Chemical analysis showed A= T, C= G
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Three groups were racing to discover the 3D shape of DNA Linus Pauling Maurice Wilkins/Rosalind Franklin James Watson/Franklin Crick
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Watson and Crick – 1953 Present their molecular model for DNA Double helix Antiparallel Hydrogen bonding between bases Nobel prize in 1962
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Watson and Crick also discovered the process of replication Copying the DNA strand Predicted that DNA was semiconservative Each new strand has a parent strand attached
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Replication begins at Origins of Replication Short, specific DNA sequences Creates a replication fork Involves several enzymes Helicases Single strand binding proteins Topoisomerases Primase
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Each strand serves as a template for new strands DNA polymerases Requires a primer of RNA to begin Strands are antiparallel 5’ – phosphate end 3’ – sugar-OH end Only add bases to the 3’ end – BUT must go 5’ – 3’ – problem?
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Two strands will exist when replication begins Leading strand DNA polymerase III at fork adds nucleotides towards the fork Requires one primer Lagging strand Made as a series of segments
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Lagging Strand Requires multiple RNA primers DNA pol III adds nucleotide to RNA primer – Okazaki fragment DNA pol I adds DNA to replace RNA primer at junction of Okazaki fragments DNA ligase bonds the pieces of DNA
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Errors in replication occur about 1 in 10 billion Mismatch repair is when enzymes remove a base that has been incorrectly placed If the change is not corrected and becomes permanent then it represents a mutation Sometimes the region where the error is located is excised by enzymes called nuclease and then new DNA place
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Replication leaves the 5’ end uncopied Telomeres are nucleotide sequences at the 3’ and 5’ ends Prevent the eroesion of genes located near an end Become shorter every round of replication Do not get shorter in germ cells - telomerase
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DNA can be up to 4 cm long in an eukaryote Combines with histone proteins to become chromatin When ready to divide the chromatin condenses into packages (chromsomes)
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