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In the 1940s, most scientists thought that protein was the genetic material because :

In the 1940s, most scientists thought that protein was the genetic material because :. there are many varieties of proteins they are very specific nobody knew much about nucleic acids DNA seemed too uniform to account for so many genetic traits

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In the 1940s, most scientists thought that protein was the genetic material because :

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  1. In the 1940s, most scientists thought that protein was the genetic material because: • there are many varieties of proteins • they are very specific • nobody knew much about nucleic acids • DNA seemed too uniform to account for so many genetic traits • Griffith’s experiment showed that the genetic material is a specific molecule.

  2. The R and S phenotypes are inherited in bacteria

  3. Conclusions: S is pathogenic R is non-pathogenic R cells could “become” S cells! The R cells had been “transformed” into S cells by acquiring genetic material from the S cells. They now give rise to new S cells when they reproduce. The process by which genetic material is transferred to bacteria is called TRANSFORMATION.

  4. Hershey and Chase’s experiments showed that DNA was the genetic material of a virus (phage) that infects bacteria. A phage consists of DNA with a protein coat around it. They labeled protein with 35S and DNA with 32P Bacterial cells were infected and then washed to get rid of the part of the phage that remained outside the bacteria.

  5. They wanted to know whether the phages inserted DNA or protein into bacteria.

  6. Conclusions: • Viral proteins remain outside host cell • Viral DNA is injected into the host cell • Injected DNA molecules cause cells to produce more viruses • Nucleic acids rather than proteins are the genetic material!

  7. Chargaff found that in DNA # of adenines = # of thymines AND # of cytosines = # of guanines

  8. By looking at an X-ray crystallography picture taken by Rosalind Franklin, Watson & Crick deciphered the double helical structure of DNA

  9. A always pairs with T C always pairs with G • Significance of base pairing • It explains Chargaff’s rules • It suggests the general mechanism for DNA replication • Its sequence of bases can be highly variable—good for coding genetic information • Though hydrogen bonds are weak, there are enough of them to stabilize the DNA molecule

  10. Models of DNA replication Dark blue = original (parent) DNA Light blue = new (daughter) DNA

  11. Meselson and Stahl used 15N to label DNA

  12. DNA replication is • Complex—over a dozen enzymes and other proteins are involved • 2. Extremely rapid—500 nucleotides are added/sec in prokaryotes & 6 billion bases in humans are copied in a few hours • 3. Very accurate—only about 1 in 10 billion nucleotides is paired incorrectly

  13. Basic Steps of DNA Replication • Double helix untwists with the help of helicase, and base pairs separate. • 2. Each “old” strand is a template, and new nucleotides are added according to the base-pairing rules. • 3. Nucleotides are connected (ligated) to form sugar-phosphate backbones. • 4. Now we have 2 new DNA molecules, each having 1 “old” strand and 1 “new” strand.

  14. Origins of Replication– where replication begins (prokaryotes have 1, eukaryotes have many) Replication proceeds in both directions.

  15. DNA polymerase adds nucleotides to the new strand of DNA at the replication fork.

  16. DNA polymerase can’t intitiate elongation. Primase lays down an RNA primer to which DNA pol can add. The primer is later replaced with DNA.

  17. DNA strands are ANTIPARALLEL 5’ end = P 3’ end = OH DNA polymerase can only add on to the 3’ end! So new DNA can ONLY be made 5’ 3’ 3’ 5’ 3’ 5’ Direction of Replication

  18. Leading strand can elongate continuously in the 5’ 3’ direction. But the lagging strand has to grow in short segments = Okazaki fragments

  19. Ligase joins the Okazaki fragments together.

  20. DNA Pol III adds nucleotides to the growing strand DNA Pol I replaces the RNA primer

  21. Mistakes are made in DNA replication, but they’re usually repaired quickly. DNA pol can recognize the mistake, go back, and fix it. • If DNA is damaged later, it’s fixed by excision repair. • Nuclease cuts out damaged piece of DNA • DNA pol fills in the gap • DNA ligase seals it

  22. At the 5’ ends of the lagging strands on each chromosome, the RNA primer can’t be replaced. Each time the chromosome is replicated, it gets shorter since single stranded DNA is unstable. Prokaryotes don’t have this problem since they have circular DNA.

  23. Eukaryotes have telomeres at the ends-TTAGGG sequences- that are repeated 100-1000 times. They don’t code for anything, so the DNA can replicate many times before an actual gene is affected.

  24. Telomerase can lengthen telomeres, but it’s not present in most of our cells (only in germ cells that produce gametes). In fact, telomerase has been found to be present in cancerous cells

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