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Minot State University Genetics Biol 215

Minot State University Genetics Biol 215. Spring 2013 Heidi Super. Lecture 33 April 24 th , 2013 . ANNOUNCEMENTS ! YIKES! No class on Friday. I forgot to announce on Monday. I apologize. ND academy of science mtg.

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Minot State University Genetics Biol 215

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  1. Minot State UniversityGeneticsBiol 215 Spring 2013 Heidi Super

  2. Lecture 33 April 24th, 2013 ANNOUNCEMENTS! YIKES! No class on Friday. I forgot to announce on Monday. I apologize. ND academy of science mtg. Use this time to review and study the last section of material. Exam 4 next Wednesday. We are in the final stretch of the course! Stay up to date. Review lectures. Keep coming in for help/discussion of concepts. Organize your time!

  3. Lab reports---Instead of a standard lab report, I would like you to research the use of GFP in some other application See handout for more instruction. Due Thursday in Lab • New lab protocol will be posted today. 2-part lab, will finish next week.

  4. F2 Flies • Amazing job on flies. 12 students done! There will be plenty of flies for all. The cultures are really healthy and packed with larva and pupae. Flies will keep emerging into early next week! To be as fair as possible, please limit each counting session to the flies in 2 vials. That leaves some flies for more students each day.

  5. The Excel file for the data is saved on the desktop of the computer. Keep adding to the data. You may want to wait until you have counted ~100 flies. • Turn in your sheet with your individual data to me as soon as you finish.

  6. Where were we? • DNA replication • Where does DNA replication begin in a DNA molecule? • What kind of proteins have to work together to produce a new strand of DNA? • How do antiparallel strands get copied together? • Summarize the process

  7. Helper proteins Table 11.4

  8. Pay special attention to the orientation of the template strands when sketching the leading and lagging strand in the process of replication.

  9. Figure 11.11

  10. Short fragments of DNA made from the lagging strand, called Okasaki fragments. • Eventually primers are removed and Okasaki fragments are linked into a continuous strand of DNA. (Role of DNA pol I in prokaryotes like E. coli) (Details coming!) • This extra work takes time so the synthesis lags behind the continuous synthesis.

  11. View this animation(also found on website) • http://www.wiley.com/college/pratt/0471393878/student/animations/dna_replication/index.html • It is an excellent review!!!!!

  12. Let’s look closer at one replication fork. Recall both strands are being copied simultaneously and the polymerase enzymes are moving in one overall direction. • Current model for how this might work.

  13. Figure 11.12

  14. A more detailed look showing the relative positions of the helper proteins at a replication fork. Study and re-sketch! Figure 11.13

  15. An actual replication fork

  16. Bacteria like E. coli have a single origin of replication which creates one replication bubble which forms two replication forks.

  17. Study this!

  18. Eukaryotic cells have linear chromosomes which have multiple ARS sequences. Many replication bubbles form. Each bubble makes 2 replication forks.

  19. Discontinuous replication… • Obviously the lagging strand cannot be left as small unlinked fragments of DNA. • The primary role of DNA polymerase I is the removal of RNA primers and simultaneous replacement with DNA.

  20. Figure 11.16

  21. DNA polymerase cannot link the individual Okasaki fragments, however. • Role of yet another helper protein called DNAligase. Lagging strand template Okasaki fragment 1 Okasaki fragment 2 DNA ligase—makes the phosphodiester bond

  22. One final detail… • All DNA polymerases can occasionally make mistakes when reading the DNA template. 3’AGCCTCGAACGGTAATT…..(template) 5’TCGGAGCTTA DNA polymerase III makes a mistake, adding A instead of G DNA polymerase III

  23. DNA polymerase III has built-in proofreading and error correction activity. 3’AGCCTCGAACGGTAATT…..(template) 5’TCGGAGCTTG DNA polymerase III corrects its mistake, replacing A with G before moving on to next nucleotide DNA polymerase III

  24. Observe replication animations on website.

  25. What about linear chromosomes?... • A problem arises with primed replication at DNA ends. • Let’s revisit a slide

  26. Figure 11.16

  27. After each round of replication, the lagging strand has an unfilled gap, where primers are removed, but if no adjacent Okasaki fragment exists, the gap cannot be filled. • Since this strand serves as template in the next round of replication there is potential for continued shortening of each linear chromosome.

  28. The solution? Telomeres! • Telomeres are sections of DNA at the ends of linear chromosomes that you don’t inherit from your parents. • Telomeres are created by an enzyme called telomerase (clever name huh?)

  29. Telomerase is an interesting enzyme which uses its own built in template to copy short repeats which are added to the ends of the inherited DNA. • The template is actually RNA!

  30. What do telomeres actually do? • They serve as a protection against loss of important DNA due to this replication problem. • Shortening of the ends of the chromosomes is fine if it just removes some telomere repeats. • Shortening of the ends of chromosomes is NOT FINE if it removes genes that encode essential proteins!

  31. Telomeres are also indicators of the age of a cell/organism • Telomerase is active during development of an organism, but later stops working. • In other words, our cells do not keep adding telomere repeats to chromosomes throughout our lifetime.

  32. So our chromosomes continue to shorten with every round of replication. As long as the shortening does not remove essential genes, there is not problem. • But the shortening serves as an indicator of the number of rounds of replication and then cell division that has taken place.

  33. The more rounds of replication, the shorter the chromosomes. • This shortening actually helps a cell know when it is too old to safely remain a part of the organism. • A cell that senses it has short chromosomes is normally triggered to undergo apoptosis.

  34. The shortening of telomeres is a safety mechanism to reduce the accumulation of cells with DNA that may have accumulated mutations with many rounds of replication. • The older the cell in the body, the shorter the chromosomes…

  35. Seems like a silly thing to focus on…the length of chromosomes. • Why are telomeres so important? • A nobel prize was recently shared by 3 individuals whose life work has explained how telomeres work.

  36. Active telomerase is found in lots of cancer cells! • Recall adults are not supposed to keep making telomerase. This insures that chromosomes shorten and that older cells eventually die by apoptosis. • Active telomerase confuses the system. Cells lose track of their age and are allowed to divide too many times.

  37. Where are we headed? Monday---One last lecture just introducing gene expression Topics list for exam 4—Next Wednesday. Final Lab next Thursday Final exam

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