1. 1. What is the Central Dogma? 2. How does prokaryotic DNA compare to eukaryotic DNA? 3. How is DNA organized in eukaryotic cells?

2. 1. Draw and label the 3 parts of an operon. 2. Contrast inducible vs. repressible operons. 3. How does DNA methylation and histone acetylation affect gene expression?

3. 1. Compare DNA methylation and histone acetylation. 2. What is the role of activators vs. repressors? Where do they bind to? 3. List the components found in a eukaryotic transcription initiation complex. 4. What is the function of miRNAs and siRNAs?

4. 1. List and describe the 3 processes that are involved in transforming a zygote. 2. Compare oncogenes, proto-oncogenes, and tumor suppresor genes. 3. What are the roles of the ras gene and the p53 gene?

5. Chapter 18

6.  Genes can be activated by inducer molecules, or they can be inhibited by the presence of a repressor as they interact with regulatory proteins or sequences.  A regulatory gene is a sequence of DNA that codes for a regulatory protein such as a repressor protein.  How the components of an operon function to regulate gene expression in both repressible and inducible operons.  How positive and negative control function in gene expression.  The impact of DNA methylation and histone acetylation on gene expression.  How timing and coordination of specific events are regulated in normal development, including pattern formation and induction.  The role of miRNAs in control of cellular functions.  The role of gene regulation in embryonic development and cancer.

7. Transcription

9. Operon Operon: cluster of related genes with on/off switch Three Parts: 1.Promoter – where RNA polymerase attaches 2.Operator – “on/off”, controls access of RNA poly 3.Genes – code for related enzymes in a pathway

10. Regulatory generepressor Regulatory gene: produces repressor protein that binds to operator to block RNA polymerase

12.  Normally ON  Anabolic (build organic molecules)  Organic molecule product acts as corepressor  binds to repressor to activate it  Operon is turned OFF trp operon  Eg. trp operon

13. trp operon

14.  Normally OFF  Catabolic (break down food for energy) inducer  Repressor is active  inducer binds to and inactivates repressor  Operon is turned ON lac operon  Eg. lac operon

15. lac operon

16. off  Negative control: operons are switched off by active form of repressor protein ◦ Eg. trp operon, lac operon increase  Positive control: regulatory protein interacts directly with genome to increase transcription ◦ Eg. cAMP & CAP

17.  cAMP: accumulates when glucose is scarce  cAMP binds to CAP (catabolite activator protein)  Active CAP  binds to DNA upstream of promoter, ↑ affinity of RNA polymerase to promoter, ↑ transcription

18. Many stages

19.  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 differential gene expression  Differences between cell types is due to differential gene expression

21. 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

23.  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  Eg. DNA methylation (gene silencing), histone acetylation, X chromosome inactivation, heterochromatin (silent chromatin)

24. Genetic Science Learning Center

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

26. Activators bind to enhancer regions + other proteins + RNA polymerase

27. Cell type-specific transcription

28. Regulation of mRNA: micro RNAs (miRNAs) small interfering RNAs (siRNAs) micro RNAs (miRNAs) and small interfering RNAs (siRNAs) can bind to mRNA and degrade it or block translation

34. Genetic Science Learning Center

35. Section 18.4

36. 1. Cell Division: large # identical cells through mitosis 2. Cell Differentiation: cells become specialized in structure & function 3. Morphogenesis: “creation of form” – organism’s shape

38.  Cytoplasmic determinants: maternal substances in egg distributed unevenly in early cells of embryo

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

44. HHMI Short Film

45. Stickleback FishHumans  Development of pelvic bone  Development of anterior structures, brain, structure of hindlimb  Mutation may cause clubfoot, polydactyly (extra fingers/toes), upper limb deformities

46.  Most of the embryonic cells are produced in excess apoptosis  Cells will undergo apoptosis (programmed cell death) to sculpture organs and tissues caspase  Carried out by caspase proteins

47. Section 18.5

48. 1. Proto-oncogene = stimulates cell division 2. Tumor-suppressor gene = inhibits cell division  Mutations in these genes can lead to cancer

49. Proto-OncogeneOncogene  Gene that stimulates normal cell growth & division  Mutation in proto- oncogene  Cancer-causing gene Effects:  Increase product of proto-oncogene  Increase activity of each protein molecule produced by gene

51.  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

52.  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

55.  Embryonic development occurs when gene regulation proceeds correctly  Cancer occurs when gene regulation goes awry