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Review Warm-Up

Understand the central dogma of gene expression, compare prokaryotic and eukaryotic DNA organization, and learn about the regulation of gene expression in bacteria and eukaryotes.

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Review Warm-Up

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  1. Review Warm-Up • What is the Central Dogma? • How does prokaryotic DNA compare to eukaryotic DNA? • How is DNA organized in eukaryotic cells?

  2. Ch. 18 Warm-Up • Draw and label the 3 parts of an operon. • Contrast inducible vs. repressible operons. • How does DNA methylation and histone acetylation affect gene expression?

  3. Ch. 18 Warm-Up • Compare DNA methylation and histone acetylation. • What is the role of activators vs. repressors? Where do they bind to? • List the components found in a eukaryotic transcription initiation complex. • What is the function of miRNAs and siRNAs?

  4. Ch. 18 Warm-Up • List and describe the 3 processes that are involved in transforming a zygote. • Compare oncogenes, proto-oncogenes, and tumor suppresor genes. • What are the roles of the ras gene and the p53 gene?

  5. Regulation of Gene Expression Chapter 18

  6. Regulation of Gene Expression by Bacteria Transcription

  7. Regulation of metabolic pathways • Bacteria has a unique way of synthesizing the amino acid tryptophan. An abundance of tryptophan can inhibit the synthesis of other enzymes that are necessary for gene replication.

  8. Bacterial control of gene expression Operon: cluster of related genes with on/off switch Three Parts: • Promoter – where RNA polymerase attachedlocated immediately adjacent to gene, a recognition starting point. • Operator – “on/off”, controls access of RNA poly • Genes – code for related enzymes in a pathway

  9. Regulatory gene: produces repressorprotein that binds to operator to block RNA polymerase

  10. Repressible Operon (ON  OFF) Inducible Operon (OFF  ON)

  11. Repressible Operon • Normally ON • Anabolic (build organic molecules) • Organic molecule product acts as corepressor binds to repressor to activate it • Operon is turned OFF • Eg. trpoperon

  12. Inducible Operon • Normally OFF • Catabolic (break down food for energy) • Repressor is active inducerbinds to and inactivates repressor • Operon is turned ON • Eg. lacoperon

  13. Gene Regulation:Positive vs. Negative Control • Negative control: operons are switched offby active form of repressor protein • Eg. trp operon, lac operon • Positive control: regulatory protein interacts directly with genome to increasetranscription • Eg. cAMP (cyclic adenosine monophosphate & CAP (catabolic activator protein)

  14. Gene Regulation • The lac operon is negatively regulated by a repressor protein: • lac repressor binds to the operator to block transcription • in the presence of lactose, an inducer molecule binds to the repressor protein • repressor can no longer bind to operator • transcription proceeds

  15. Trp and lac operon • https://www.youtube.com/watch?v=EvLy_1_Y3tk

  16. Regulation of Gene Expression by Eukaryotes Many stages

  17. Typical human cell: only 20% of genes expressed at any given time • Different cell types (with identical genomes) turn on different genes to carry out specific functions • Differences between cell types is due to differential gene expression

  18. Chromatin Structure: • Tightly bound DNA  less accessible for transcription • DNA methylation: methyl groups added to DNA; tightly packed;  transcription • Histone acetylation: acetyl groups added to histones; loosened;  transcription

  19. Transcription Initiation: • Specific transcription factors (activators or repressors) bind to control elements (enhancer region) • Activators: increase transcription • Repressors: decrease transcription

  20. Cell type-specific transcription

  21. Video: The Epigenome at a Glance Genetic Science Learning Center

  22. Epigenetic Inheritance • Modifications on chromatin can be passed on to future generations • Unlike DNA mutations, these changes to chromatin can be reversed (de-methylation of DNA) • Explains differences between identical twins

  23. Epigenetics of Identical Twins • https://www.youtube.com/watch?v=oqAbymytqdU Ms. Grayson’s Identical Twin Brothers

  24. Summary of Eukaryotic Gene Expression

  25. Embryonic Development of Multicellular Organisms Section 18.4

  26. Embryonic Development:Zygote  Organism • Cell Division: large # identical cells through mitosis • Cell Differentiation: cells become specialized in structure & function • Morphogenesis: “creation of form” – organism’s shape

  27. Determination: irreversible series of events that lead to cell differentiation

  28. Cytoplasmic determinants: maternal substances in egg distributed unevenly in early cells of embryo that impacts its development.

  29. Induction: cells triggered to differentiate • Cell-Cell Signals: molecules produced by one cell influences neighboring cells • Eg. Growth factors

  30. Pattern formation: setting up the body plan (head, tail, L/R, back, front)

  31. Morphogens: substances that establish an embryo’s axes

  32. Homeotic genes: master control genes that control pattern formation (eg. Hox genes)

  33. Evolving Switches, Evolving Bodies HHMI Short Film

  34. Pitx1 Gene = Homeotic/Hox Gene • Development of pelvic bone • Development of anterior structures, brain, structure of hindlimb • Mutation may cause clubfoot, polydactyly (extra fingers/toes), upper limb deformities Stickleback Fish Humans

  35. Role of Apoptosis • Most of the embryonic cells are produced in excess • Cells will undergo apoptosis(programmed cell death) to sculpture organs and tissues • Carried out by caspaseproteins

  36. Cancer results from genetic changes that affect cell cycle control Section 18.5

  37. Control of Cell Cycle: • Proto-oncogene = stimulates cell division • Tumor-suppressor gene = inhibits cell division • Mutations in these genes can lead to cancer

  38. Gene that stimulates normal cell growth & division • Mutation in proto-oncogene • Cancer-causing gene Effects: • Increase productof proto-oncogene • Increase activityof each protein molecule produced by gene Proto-Oncogene Oncogene

  39. Proto-oncogene  Oncogene

  40. Genes involved in cancer: • Ras gene: stimulates cell cycle (proto-oncogene) • Mutations of ras occurs in 30% of cancers • p53 gene: tumor-suppresor gene • Functions: halt cell cycle for DNA repair, turn on DNA repair, activate apoptosis (cell death) • Mutations of p53 in 50+% of cancers

  41. Cancer results when mutations accumulate (5-7 changes in DNA) • Active oncogenes + loss of tumor-suppressor genes • The longer we live, the more likely that cancer might develop

  42. Viruses and Cancer • Viruses may at first seem very different from mutations as a cause of cancer. • However, we now know that viruses can interfere with gene regulation in several ways if they integrate their genetic material into the DNA of a cell.

  43. Summary • Embryonic development occurs when gene regulation proceeds correctly • Cancer occurs when gene regulation goes awry

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