23 Exam 3 Study Guide

The following are suggestions of what you should study for each RIQ and Exam in BS161.

RIQ 017-018

1. Draw a model showing the key components of cell signaling pathways. Give specific examples of these components in G protein-coupled receptor and receptor kinase pathways. (See PCA Cell communication, part B.)
2. Draw a table showing the key mechanisms of cell signaling (how each is activated and terminated). Give specific examples of these mechanisms in G protein-coupled receptor and receptor kinase pathways as applicable (some mechanisms are only found in one type of pathway). (See PCA Cell communication, part D.)
3. Draw a model showing the actions of kinases and phosphatases. On the model, label all reactants (substrates), the enzyme, and the products of the reaction. Give specific examples of this reaction in the G protein-coupled receptor and receptor kinase pathways. (See ICA Cell communication.)
4. Draw a model showing the activation and inactivation of a G protein. Give specific examples of this reaction in the G protein-coupled receptor and receptor kinase pathways. (See ICA Cell communication.)
5. Draw a model showing the signaling in response to a steroid hormone and the typical cellular response observed. Contrast this pathway with the pathways involving cell-surface receptors in terms of the ligand properties, signaling proteins, ability for signal amplification, and the cellular response. (See PCA Cell communication, part E, and ICA Cell communication, Activities 2 and 3).
6. Draw a table showing the key events and features of each phase of the cell cycle (G₁, S, G_2, and M phase) and the G₀ phase. Specifically describe how and why the amount of DNA at each phase changes. (See PCA Cell cycle, part D.)
7. Draw a model of a cell with two non-homologous chromosomes before and after replication. Label all membranes, centromeres, and sister chromatids when present. (See PCA Cell cycle, part E., ICA Cell cycle, activity 1.)
8. Draw a model of a cell with two non-homologous chromosomes in metaphase of M phase and in G₀, after M phase is complete. Label all membranes, spindle fibers, centromeres, and sister chromatids when present. (See ICA Cell cycle, activity 2.)
9. Draw a graph showing the number of cells present in a typical population vs the amount of DNA per cell. Label the regions representing G₁/G₀, S, and G₂/M phase on this graph. (See PCA Cell cycle, part F.) Use the graph to explain how changes in cell cycle steps would be reflected in the graph. (See ICA Cell cycle, activity 3.)

RIQ 019-020

1. Draw a model of inactive CDK, active CDK, and active CDK carrying out its function. Explain how and why active CDK relates to progress through the cell cycle (See PCA Cell cycle regulation, part 2, and ICA Cell cycle regulation, activity 1.)
2. Draw a table showing proteins and/or protein complexes needed to progress to the next phase of the cell cycle. Specifically describe what events occur in response to the active protein or protein complex, and what would pause the cell at each phase. Classify the proteins in this table as having proto-oncogenic or tumor suppressor function, based on their effect on the cell cycle. (See PCA Cell cycle regulation, parts 3 & 4, and ICA Cell cycle regulation, activities 2 and 4.)
3. Draw a model of cell cycle events integrated with regulators of those events. (See PCA Cell cycle regulation, part 5.)
4. Draw a table listing the key enzymes for DNA replication and their functions. Use this information to predict what would be different if a given enzyme did not carry out its function. (See PCA DNA replication, part E.)
5. Draw a model of a replication bubble with RNA primers and the first few nucleotides produced by DNA polymerase next to each primer. (See ICA DNA replication, Activities 1 and 2.)
   1. Use arrows and labels to show where enzymes from #1 act during the process of initiating replication.
   2. Label the leading and lagging strands at each fork.
6. Draw a model of a cell with two chromosomes dividing in the presence of labeled nucleotides. Show the appearance of the chromosomes after one and two divisions. Explain how the models demonstrate semi-conservative replication. (See ICA DNA replication, Activity 3.)

RIQ 021-022

1. Define mutation, and explain how DNA damage is different from a mutation.
2. Name two events that can lead to mutations.
3. Use your knowledge of DNA structure to describe the general approach for detecting and repairing the following types of errors/DNA damage. If damage is not likely to be correctly repaired, explain why.
   1. Replication errors detected by DNA polymerase as it is synthesizing DNA.
   2. Replication errors detected by proteins other than DNA polymerase during S phase.
   3. Depurination of an adenine nucleotide in G₀.
   4. Deamination of cytosine to uracil in G₀.
   5. Deamination of 5-methylcytosine to thymine in G₀.
4. Draw a table to illustrate the effect of synonymous, missense, nonsense, and frameshift mutations on mRNA and amino acid sequences. (See PCA DNA damage and mutations.)
5. Give examples of mutations that would have the following effects on protein structure (hint: refer to the codon table, the amino acid structures, and your table of bonds and forces). Explain which of these would most likely affect the function of the protein. (See PCA Bonds and forces, PCA Gene expression II, PCA CC gene expression & protein structure.)
   1. A specific mutation that would not alter the primary protein structure
   2. A specific mutation that would alter the primary protein structure but likely not the tertiary structure
   3. A specific mutation that would alter the primary protein structure and likely the tertiary structure
6. Draw models of the Receptor Kinase pathway linked to a growth factor ligand under each of the following conditions and explain each step: (See ICA Model of Ras and cancer.)
   1. Growth factor ligand is present, Ras is healthy, no drug
   2. Growth factor ligand is absent, Ras is healthy, no drug
   3. Growth factor ligand is absent, Ras is mutated such that Ras is slow to hydrolyze GTP, no drug
   4. Growth factor ligand is absent, Ras is mutated such that Ras is slow to hydrolyze GTP, drug that inhibits the function of Ras is present
7. For each of the above conditions, explain how the cell cycle is affected and why, referring to cyclin D expression, CDK function, and the role of cyclin-CDK complexes in the process of cell division. (See ICA Model of Ras and cancer.)