Final Exam Review Guide
Final Exam Review Guide BIOL01203
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This 8 page Study Guide was uploaded by Maya Panchal on Wednesday March 30, 2016. The Study Guide belongs to BIOL01203 at Rowan University taught by Dr. Demarest in Fall 2015. Since its upload, it has received 23 views. For similar materials see Biology 3: Cell Biology in Biology at Rowan University.
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Date Created: 03/30/16
Biology III Final Exam Study Guide -Know the different types of junctions and their functions - Know the ways that DNA damage can be repaired – during DNA replication & after DNA replication – exonucleases versus endonucleases – know the role of methylation in the repair process, thymine dimers, DNA polymerase During DNA replication: After DNA replication: Excision repair-Repair endonucleases are recruited to DNA by proteins that recognize damage 1. They cleave the backbone adjacent to the damage site; other enzymes remove the defective nucleotides 2. DNA polymerase replaces the missing nucleotides 3. DNA ligase seals the remaining nick in the repaired strand Types of excision repair • Excision repair pathways are classified into two types • Base excision repair corrects single damaged bases - The sugar with the missing base is then recognized by a repair endonuclease that detects depurination • It breaks the phosphodiester backbone to one side of the sugar and a second enzyme removes the sugar Biology III Final Exam Study Guide Proofreading • Exonucleases degrade nucleic acids from the ends of the molecules - The exonuclease activity of DNA polymerase allows it to remove incorrectly base- paired nucleotides and incorporate the correct base • Endonucleases make internal cuts in nucleic acid molecules Nucleotide excision repair For removing pyrimidine dimers and other bulky lesions, a second type of excision repair is employed Nucleotide excision repair uses proteins that detect distortions in the DNA helix and recruit NER endonuclease that cuts the DNA backbone on either side of the lesion Helicase unwinds the DNA between the nicks, and frees it from the DNA; DNA polymerase and ligase complete the repair The NER system is versatile The nucleotide excision repair system detects and corrects many types of DNA damage Sometimes it is recruited to regions where transcription is stalled because of DNA damage; this is called transcription-coupled repair Mismatch Repair Corrects Mutations That Involve Noncomplementary Base Pairs • Mismatch repair targets errors made during DNA replication that escape proofreading • Mismatch repair is able to distinguish the original vs. the newly synthesized strand in order to correctly repair the mismatch Methylation in mismatch repair • DNA methylation does not occur immediately after DNA replication • Therefore, mismatch repair systems can distinguish the original DNA (methylated) from the newly made strand (non- methylated) • The incorrect nucleotide in the newly made strand is excised and replaced Biology III Final Exam Study Guide Damage Repair Helps Explain Why DNA Contains Thymine Instead of Uracil For some years it was not clear why DNA contained thymine instead of uracil But repair of deaminated nucleotides shows why DNA cannot contain uracil Deamination of cytosine converts it to uracil, which is detected and repaired; if DNA contained uracil normally, this type of repair could not be effected Double-Strand DNA Breaks Are Repaired by Nonhomologous End- Joining or Homologous Recombination • Double-strand breaks cleave DNA into two fragments • It is difficult for the repair system to identify and rejoin the correct broken ends without loss of nucleotides • Two pathways are used: nonhomologous end- joining and homologous recombination -Know the functions of telomeres Telomeres Solve the DNA End- Replication Problem • Linear DNA molecules have a problem in completing DNA replication on the lagging strand, because primers are required • Each round of replication would end with the loss of some nucleotides from the ends of each linear molecule • Eukaryotes solve this problems with telomeres, highly repeated sequences at the ends of chromosomes • These noncoding sequences ensure that the cell will not lose important genetic information if DNA molecules shorten during replication - Be able to label the cell cycle restriction points and what influences them Figure 19- 12 Biology III Final Exam Study Guide - Know how G1 cyclin/CDK complexes regulate Rb/E2F function and the result – be able to explain this process Biology III Final Exam Study Guide -Cyclin gets phosphorylated by Ras, activates growth factors which activate Ras which activate cyclin cdk complex, which can phosp rbate which releases e2f, and you get transcription and S phase -G1 cyclins are required for passage through the G1 restriction point (or Start) and the Cdks to which they bind are called G1 Cdks - Know how p53 is activated during the cell cycle and what two outcomes are possible – know the signaling pathways (you do not have to know how PUMA induces apoptosis, just that it does) DNA damage activates dna damage proteins activates p53, -can result in cell cycle arrest or apoptosis, pauses the cell cycle to try to allow cell to repair, does this by activating p21, which blocks cdk, and Rb protein cannot be phosphorylated, will result in cell cycle arrest, will induce puma which results in apoptosis Biology III Final Exam Study Guide - Difference between a benign and malignant tumor •Benign tumors grow in a confined local area and are rarely dangerous •Malignant tumors (cancerous) can invade surrounding tissues, and spread throughout the body -“Seed & soil” hypothesis of cancer metastasis In the soil-microenvironment surrounding the cells, the soil is signaling to the cancer cell, sending signals to make it grow, binds and attaches more in certain areas than others. Circulating cancer cells have an affinity for the environment provided by particular organs, only some sites provide an optimal environment for their growth. Biology III Final Exam Study Guide - Know & describe the 6 hallmarks of cancer and 4 main causes Carcinogenesis is the multistep process that converts normal cells into cancer cells The four main causes of cancer are chemicals, radiation, infectious agents, heredity Six traits have been described as the hallmarks of cancer; these traits uncouple cancer cells from the normal limits on proliferation and growth The hallmarks of cancer 1. Self-sufficiency in growth signals – Normal cells require growth cells to proliferate, but cancer cells escape this requirement 2. Insensitivity to antigrowth signals – Normal tissues are protected from overproliferation by a variety of inhibitory signals, but cancer cells are insensitive to these signals 3. Apoptosis Evasion – Apoptosis is used by normal cells to prevent damaged or defective cells from continuing to divide; apoptosis is inhibited or disrupted in cancer cells 4. Limitless replicative potential – Normal cells have limited replicative potential due to telomere loss; cancer cells contain active telomerase (or other mechanisms) to maintain telomeres 5. Sustained angiogenesis – Tumor cells cannot grow beyond a few mm without a blood supply; cancer cells trigger angiogenesis by activating genes coding for angiogenesis stimulators and inhibiting genes coding for angiogenesis inhibitors 6. Tissue invasion and metastasis – Cancercellsloseadhesivenesswithneighbors,invade nearby tissues, and eventually metastasize around the body via the circulatory system Biology III Final Exam Study Guide
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