Cell Biology Final Exam Study Guide – Step-by-Step Guidance

Study Guide - Smart Notes

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Q1. How do the structure and function of epithelial tissue and connective tissue differ? Compare and contrast the structure and function of the major types of cell-cell and cell-ECM attachments in animal cells.

Background

Topic: Cell and Tissue Structure

This question tests your understanding of the differences between epithelial and connective tissues, as well as the various ways cells attach to each other and to the extracellular matrix (ECM) in animal tissues.

Key Terms and Concepts:

Epithelial tissue: Sheets of tightly connected cells that cover surfaces and line cavities.
Connective tissue: Tissues with fewer cells and abundant ECM, providing structural and metabolic support.
Cell-cell junctions: Tight junctions, adherens junctions, desmosomes, gap junctions.
Cell-ECM junctions: Hemidesmosomes, focal adhesions.

Step-by-Step Guidance

Start by describing the general structure and function of epithelial tissue (e.g., cell arrangement, polarity, presence of a basement membrane, barrier and absorption roles).
Describe the structure and function of connective tissue (e.g., cell types, ECM composition, roles in support and transport).
List and briefly define the major types of cell-cell junctions (tight junctions, adherens junctions, desmosomes, gap junctions) and cell-ECM junctions (hemidesmosomes, focal adhesions).
Compare and contrast how these junctions contribute to tissue structure and function, noting which are more prominent in epithelial vs. connective tissues.

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Q2. What roles do cadherins play in normal epithelial cells and cancer cells? What are the functions of desmosomal cadherins? What other proteins and/or structures do they each interact with inside or outside of cells? What happens if these proteins have loss of function mutations? Provide examples to support your answer.

Background

Topic: Cell Adhesion Molecules

This question focuses on the roles of cadherins (especially in cell-cell adhesion), their interactions, and the consequences of their dysfunction, particularly in disease contexts like cancer.

Key Terms and Concepts:

Cadherins: Calcium-dependent adhesion proteins important for cell-cell junctions.
Desmosomal cadherins: Specialized cadherins (desmogleins, desmocollins) in desmosomes.
Loss of function (LOF) mutations: Mutations that reduce or eliminate protein function.

Step-by-Step Guidance

Explain the role of cadherins in maintaining epithelial tissue integrity and how they mediate cell-cell adhesion.
Discuss how cadherin function changes in cancer cells (e.g., loss of E-cadherin and its effect on metastasis).
Describe the specific functions of desmosomal cadherins and their importance in tissue strength.
List the main proteins and structures that cadherins and desmosomal cadherins interact with (e.g., catenins, intermediate filaments).
Discuss the consequences of loss of function mutations in these proteins, providing at least one disease example.

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Q3. Give examples of transient cell-cell adhesion and indicate what molecules mediate these processes.

Background

Topic: Cell Adhesion Dynamics

This question tests your knowledge of temporary (transient) cell-cell interactions and the molecules involved in mediating these contacts.

Key Terms and Concepts:

Transient adhesion: Short-lived cell-cell contacts, often important in immune responses or development.
Adhesion molecules: Selectins, integrins, immunoglobulin superfamily CAMs.

Step-by-Step Guidance

Define what is meant by transient cell-cell adhesion and contrast it with stable adhesion.
List at least two biological processes where transient adhesion is important (e.g., leukocyte extravasation, neural development).
Identify the main classes of molecules that mediate these transient interactions and give specific examples.

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Q4. Discuss the structure and roles of tight junctions and gap junctions. What are the roles of claudins and connexins?

Background

Topic: Intercellular Junctions

This question examines your understanding of two key types of cell junctions and the proteins that form them.

Key Terms and Concepts:

Tight junctions: Seal spaces between epithelial cells, controlling paracellular transport.
Gap junctions: Channels that allow direct communication between cells.
Claudins: Major structural proteins of tight junctions.
Connexins: Proteins that assemble into gap junction channels.

Step-by-Step Guidance

Describe the structure and function of tight junctions, including their role in tissue barriers.
Explain the structure and function of gap junctions, focusing on cell-cell communication.
Discuss the specific roles of claudins in tight junctions and connexins in gap junctions.

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Q5. What are the three classes of ECM molecules in animal cells? Indicate their general functions and provide examples for each class. Discuss the structure of collagen and the process of collagen assembly. Why is Vitamin C essential in this process? What is osteogenesis imperfecta and what role does collagen play in this disease?

Background

Topic: Extracellular Matrix (ECM) and Collagen

This question covers the main components of the ECM, collagen structure and assembly, the role of Vitamin C, and the genetic disease osteogenesis imperfecta.

Key Terms and Concepts:

ECM classes: Fibrous proteins (e.g., collagen), proteoglycans, multiadhesive matrix proteins (e.g., fibronectin, laminin).
Collagen: Main structural protein in ECM.
Vitamin C: Cofactor for enzymes in collagen synthesis.
Osteogenesis imperfecta: Genetic disorder affecting collagen.

Step-by-Step Guidance

List the three main classes of ECM molecules and describe their general functions, giving one example for each.
Describe the structure of collagen (triple helix, amino acid composition).
Outline the steps of collagen assembly, including post-translational modifications.
Explain the role of Vitamin C in collagen synthesis and what happens in its absence.
Describe osteogenesis imperfecta and how collagen defects contribute to the disease.

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Q6. Explain how fibronectins, laminins and integrins mediate cell attachment. What biological processes do these proteins facilitate? What is Junctional Epidermolysis Bullosa and what role does laminin play in this disease? Compare and contrast the roles of focal adhesions and hemidesmosomes. How does the ECM affect cultured cells? What are some applications for using artificial ECM?

Background

Topic: Cell-ECM Interactions

This question explores how cells attach to the ECM, the roles of specific proteins, and the implications for disease and biotechnology.

Key Terms and Concepts:

Fibronectin, laminin: Multiadhesive ECM proteins.
Integrins: Transmembrane receptors for ECM proteins.
Focal adhesions, hemidesmosomes: Structures linking cells to ECM.
Junctional Epidermolysis Bullosa: Genetic disease affecting skin integrity.

Step-by-Step Guidance

Describe how fibronectins, laminins, and integrins interact to mediate cell-ECM attachment.
List biological processes that depend on these interactions (e.g., cell migration, tissue repair).
Explain the cause and symptoms of Junctional Epidermolysis Bullosa and the role of laminin.
Compare focal adhesions and hemidesmosomes in terms of structure and function.
Discuss how the ECM influences cell behavior in culture and give examples of artificial ECM applications.

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Q7. Discuss the role of the dystrophin-associated protein complex (DAPC) in maintaining muscle integrity. What is the specific role of dystrophin and how does the absence of dystrophin result in Duchenne Muscular Dystrophy (DMD)? Suggest a therapeutic approach that could have the potential to reduce DMD phenotypes in humans.

Background

Topic: Muscle Cell Structure and Disease

This question focuses on the molecular basis of muscle integrity, the role of dystrophin, and therapeutic strategies for DMD.

Key Terms and Concepts:

Dystrophin-associated protein complex (DAPC): Links cytoskeleton to ECM in muscle cells.
Dystrophin: Key protein in DAPC; stabilizes muscle cell membrane.
Duchenne Muscular Dystrophy (DMD): Genetic disease caused by loss of dystrophin.

Step-by-Step Guidance

Describe the structure and function of the DAPC in muscle cells.
Explain the specific role of dystrophin within the DAPC.
Discuss how the absence of dystrophin leads to DMD symptoms.
Suggest a therapeutic approach (e.g., gene therapy, exon skipping) and explain its rationale.

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Q8. What are the attributes and roles of stem cells? What is stem cell potency? Discuss the role of the stem cell niche. What factors regulate stem cell fate, proliferation, and differentiation?

Background

Topic: Stem Cell Biology

This question tests your understanding of stem cell properties, potency, the niche, and regulatory factors.

Key Terms and Concepts:

Stem cell attributes: Self-renewal, differentiation potential.
Potency: Totipotent, pluripotent, multipotent, unipotent.
Stem cell niche: Microenvironment regulating stem cell behavior.

Step-by-Step Guidance

List the defining attributes of stem cells and their biological roles.
Define stem cell potency and describe the different potency levels.
Explain the concept of the stem cell niche and its importance.
Identify factors (intrinsic and extrinsic) that regulate stem cell fate, proliferation, and differentiation.

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Q9. What is the promise of stem cell research? Do adult stem cells differ from embryonic stem cells and if so how? How can pluripotent stem cells be obtained? Is there any evidence that stem cell therapy is truly feasible?

Background

Topic: Stem Cell Applications

This question explores the potential of stem cell research, differences between stem cell types, and the feasibility of therapies.

Key Terms and Concepts:

Adult vs. embryonic stem cells: Sources, potency, ethical considerations.
Pluripotent stem cells: Cells that can give rise to most cell types.

Step-by-Step Guidance

Summarize the potential benefits of stem cell research for medicine and biology.
Compare and contrast adult and embryonic stem cells in terms of origin and potency.
Describe methods for obtaining pluripotent stem cells (e.g., from embryos, reprogramming).
Discuss current evidence for the feasibility of stem cell therapy, citing examples if possible.

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Q10. Compare and contrast reproductive cloning and therapeutic cloning. Explain how the technique of somatic cell nuclear transfer (SCNT) is performed. Discuss why the success rate of nuclear transfer is so low.

Background

Topic: Cloning Techniques

This question examines the differences between cloning types, the SCNT process, and technical challenges.

Key Terms and Concepts:

Reproductive cloning: Producing a whole organism.
Therapeutic cloning: Producing stem cells for therapy.
SCNT: Transferring a somatic nucleus into an enucleated egg.

Step-by-Step Guidance

Define reproductive and therapeutic cloning and highlight their similarities and differences.
Describe the steps involved in SCNT.
Discuss reasons for the low efficiency of nuclear transfer (e.g., epigenetic reprogramming challenges).

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Q11. How do induced pluripotent stem (iPS) cells differ from pluripotent stem cells? What are the advantages of iPS cells? How are iPS cells produced? What are the biomedical applications of iPS cells? Is there any evidence that iPS therapy is possible?

Background

Topic: Induced Pluripotent Stem Cells

This question focuses on iPS cells, their production, advantages, and applications.

Key Terms and Concepts:

iPS cells: Somatic cells reprogrammed to a pluripotent state.
Pluripotent stem cells: Embryonic or iPS cells capable of differentiating into most cell types.

Step-by-Step Guidance

Explain how iPS cells are similar to and different from embryonic pluripotent stem cells.
List the advantages of iPS cells (e.g., ethical, immunological).
Describe the process of generating iPS cells from somatic cells.
Discuss biomedical applications and current evidence for iPS cell therapy.

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Q12. What is cancer? Discuss the functions of the two classes of genes that are altered in tumor cells. What are some internal and external causes of cancer and how do they affect DNA? What must occur for a normal cell to become a cancer cell?

Background

Topic: Cancer Biology

This question covers the definition of cancer, genetic changes in tumor cells, causes of cancer, and the transformation process.

Key Terms and Concepts:

Oncogenes: Mutated genes that promote cell growth.
Tumor suppressor genes: Genes that inhibit cell division or promote apoptosis.
Mutagens: Agents that cause DNA mutations.

Step-by-Step Guidance

Define cancer and describe its main characteristics.
Explain the roles of oncogenes and tumor suppressor genes in cancer development.
List internal (e.g., replication errors) and external (e.g., chemicals, radiation) causes of cancer and how they affect DNA.
Summarize the key steps required for a normal cell to become cancerous.

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Q13. What are the hallmarks of a cancer cell? Compare normal versus tumor growth in the epithelium of skin. What is the difference between a benign tumor and a malignant tumor? How does cancer cell growth differ from normal cell growth?

Background

Topic: Cancer Cell Properties

This question examines the defining features of cancer cells and differences in growth patterns.

Key Terms and Concepts:

Hallmarks of cancer: Traits such as sustained proliferation, evasion of apoptosis, etc.
Benign vs. malignant: Non-invasive vs. invasive/metastatic tumors.

Step-by-Step Guidance

List the main hallmarks of cancer cells.
Compare normal and tumor growth in skin epithelium (e.g., organization, proliferation rate).
Define benign and malignant tumors and explain how their growth differs.
Discuss how cancer cell growth is deregulated compared to normal cells.

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Q14. What are the functions of proto-oncogenes? Discuss the various mechanisms involved in converting proto-oncogenes into oncogenes and provide examples to support your answers.

Background

Topic: Oncogene Activation

This question focuses on proto-oncogenes, their normal roles, and how they become oncogenes.

Key Terms and Concepts:

Proto-oncogenes: Normal genes that promote cell growth and division.
Oncogenes: Mutated or overexpressed proto-oncogenes causing uncontrolled growth.

Step-by-Step Guidance

Describe the normal functions of proto-oncogenes in cell signaling and growth.
List mechanisms that convert proto-oncogenes to oncogenes (e.g., point mutations, gene amplification, chromosomal translocations).
Provide at least one example for each mechanism.

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Q15. Discuss the mechanisms that can silence tumor suppressor genes. Explain the two-hit hypothesis. In terms of molecular mechanisms, how are hereditary and sporadic cancers similar? How are they different? What types of cells are mutated in hereditary cancer and sporadic cancer? What does it mean to be predisposed to getting cancer? Does being predisposed guarantee that an individual will develop cancer?

Background

Topic: Tumor Suppressor Genes and Cancer Genetics

This question explores how tumor suppressor genes are inactivated, the two-hit hypothesis, and differences between hereditary and sporadic cancers.

Key Terms and Concepts:

Tumor suppressor gene silencing: Mutation, deletion, epigenetic changes.
Two-hit hypothesis: Both alleles must be inactivated for cancer to develop.
Hereditary vs. sporadic cancer: Germline vs. somatic mutations.

Step-by-Step Guidance

List mechanisms that can silence tumor suppressor genes (e.g., mutations, methylation).
Explain the two-hit hypothesis and its significance.
Compare hereditary and sporadic cancers at the molecular level.
Discuss what it means to be predisposed to cancer and whether it guarantees disease development.

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Q16. Discuss the phases of the cell cycle. How can flow cytometry be utilized to study cell cycle? How is eukaryotic cell division controlled? What are the functions of cell cycle checkpoints? What is the restriction point? How are cell cycle controls disrupted in a cancer cell?

Background

Topic: Cell Cycle Regulation

This question covers the cell cycle phases, analytical techniques, and regulatory mechanisms.

Key Terms and Concepts:

Cell cycle phases: G1, S, G2, M.
Flow cytometry: Technique to analyze DNA content and cell cycle distribution.
Checkpoints: Control points ensuring proper cell cycle progression.

Step-by-Step Guidance

List and describe the main phases of the cell cycle.
Explain how flow cytometry can be used to study cell cycle phases.
Describe the main mechanisms controlling eukaryotic cell division (e.g., cyclins, CDKs).
Discuss the roles of cell cycle checkpoints and the restriction point.
Explain how these controls are disrupted in cancer cells.

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Q17. How do Ras and PI3K-Akt pathways affect cell proliferation and/or apoptosis? Draw out each signaling pathway with their associated proteins in order of action and discuss their functions.

Background

Topic: Cell Signaling Pathways

This question focuses on the Ras and PI3K-Akt pathways and their roles in regulating cell fate.

Key Terms and Concepts:

Ras pathway: Signaling cascade promoting proliferation.
PI3K-Akt pathway: Signaling cascade promoting survival and growth.

Step-by-Step Guidance

Outline the sequence of proteins in the Ras pathway and their roles.
Outline the sequence of proteins in the PI3K-Akt pathway and their roles.
Discuss how these pathways influence cell proliferation and apoptosis.

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Q18. What are the functions of Rb and E2F? How are Rb and E2F regulated? What roles do growth factors and the Ras pathway play in this process? How would LOF or GOF mutations in each of these proteins affect cells?

Background

Topic: Cell Cycle Regulation and Cancer

This question examines the Rb-E2F regulatory axis and its modulation by signaling pathways.

Key Terms and Concepts:

Rb (Retinoblastoma protein): Tumor suppressor controlling cell cycle progression.
E2F: Transcription factor promoting S-phase entry.
LOF/GOF mutations: Loss/gain of function mutations.

Step-by-Step Guidance

Describe the normal functions of Rb and E2F in cell cycle control.
Explain how Rb and E2F are regulated by phosphorylation and signaling pathways.
Discuss the roles of growth factors and the Ras pathway in this regulation.
Predict the effects of LOF or GOF mutations in Rb and E2F on cell proliferation.

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Q19. What are the roles and functions of p53 and p21? What regulates their expression or activity? How do cells respond to DNA damage? What happens if the damage is irreparable? How would LOF mutations in each of these proteins affect cells? Discuss the cause of Li-Fraumeni syndrome. Draw out the p53-mediated signaling pathways that cause cell cycle arrest and apoptosis. Be sure to indicate the proteins involved in their order of action and discuss the function of each of these proteins.

Background

Topic: DNA Damage Response and Tumor Suppression

This question covers the p53 pathway, its regulation, and its role in cancer predisposition syndromes.

Key Terms and Concepts:

p53: Tumor suppressor protein, "guardian of the genome".
p21: CDK inhibitor induced by p53.
Li-Fraumeni syndrome: Inherited p53 mutation syndrome.

Step-by-Step Guidance

Describe the roles of p53 and p21 in cell cycle arrest and apoptosis.
Explain how p53 and p21 expression/activity are regulated (e.g., by DNA damage).
Outline the cellular response to DNA damage, including possible outcomes.
Discuss the effects of LOF mutations in p53 and p21, and the cause of Li-Fraumeni syndrome.
Draw and describe the p53-mediated signaling pathways leading to cell cycle arrest and apoptosis, listing key proteins in order.

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Q20. Describe the major steps of apoptosis. Discuss how the mitochondria and downstream events induce apoptosis.

Background

Topic: Programmed Cell Death

This question focuses on the molecular events of apoptosis, especially the mitochondrial pathway.

Key Terms and Concepts:

Apoptosis: Programmed cell death involving caspases.
Mitochondrial pathway: Release of cytochrome c, apoptosome formation.

Step-by-Step Guidance

List the major steps of apoptosis, from initiation to cell dismantling.
Describe the role of mitochondria in apoptosis (e.g., cytochrome c release).
Explain how downstream events (e.g., caspase activation) lead to cell death.

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Q21. Explain the genetic basis of Chronic Myelogenous Leukemia (CML). Explain why imatinib/Gleevec can be used to successfully treat most patients with CML. Why might a patient no longer respond to Gleevec?

Background

Topic: Cancer Genetics and Targeted Therapy

This question examines the molecular cause of CML and the mechanism of targeted therapy.

Key Terms and Concepts:

CML: Cancer caused by the BCR-ABL fusion gene (Philadelphia chromosome).
Imatinib/Gleevec: Tyrosine kinase inhibitor targeting BCR-ABL.

Step-by-Step Guidance

Describe the chromosomal translocation that creates the BCR-ABL fusion gene in CML.
Explain how the BCR-ABL protein leads to uncontrolled cell proliferation.
Discuss how imatinib/Gleevec inhibits BCR-ABL and why this is effective in treating CML.
List possible reasons why some patients may develop resistance to Gleevec.