cell bio

Chapter 16 - Cytoskeleton

Three Main Cytoskeletal Filaments:

Microfilaments (Actin filaments): Thin, flexible filaments that support cell shape, contribute to motility (e.g., muscle contraction), and form structures like the microvilli.

Intermediate Filaments: Ropelike fibers that provide mechanical support, especially in epithelial cells, neurons, and the nuclear membrane. Examples include keratins, vimentin, and lamin.

Microtubules: Long, hollow cylinders made of tubulin that support cell shape, facilitate intracellular transport, and form structures like the mitotic spindle, cilia, and flagella.

Role of Actin: Actin is a key component of microfilaments. It is involved in cellular movements, muscle contraction, and cytokinesis.

Actin vs. Lamin: Actin forms microfilaments, while lamin forms intermediate filaments, specifically in the nuclear lamina.

Diseases from Mutations in Actin: Actin mutations can cause defects in cell movement, immune function, and muscle contraction (e.g., cardiac and skeletal muscle disorders).

Myosin and Actin: Myosin is a motor protein that interacts with actin filaments in muscle cells. Myosin uses ATP hydrolysis to generate force for muscle contraction.

Role of Calcium in Muscle Contraction: Calcium ions bind to troponin on actin filaments, leading to conformational changes that allow myosin heads to interact with actin and contract the muscle.

Microtubules: Composed of tubulin, microtubules are rigid and essential for intracellular transport (via kinesin and dynein motor proteins), cell division (spindle formation), and structure (cilia and flagella).

Diseases from Microtubule Mutations: Issues like neurodegenerative diseases can occur, such as when motor proteins like dynein or kinesin are malfunctioning.

Intermediate Filaments: These are rope-like fibers and include proteins like keratin (in epithelial cells), vimentin (in mesenchymal cells), and lamin (in the nuclear membrane).

Diseases: Mutations can cause epidermolysis bullosa (due to keratin defects) or neurodegenerative disorders (due to vimentin or lamin mutations).

Chapter 17 - Cell Cycle

Mitosis vs. Meiosis:

Mitosis: Somatic cell division for growth and repair, producing two genetically identical daughter cells.

Meiosis: Reproductive cell division that reduces chromosome number by half, resulting in four non-identical haploid cells.

Two Major Phases of the Cell Cycle:

Interphase: The cell grows and DNA is replicated (G1, S, G2).

M Phase: The cell divides (mitosis or meiosis) and then undergoes cytokinesis.

Four Subphases of the Cell Cycle:

Interphase: G1 (cell growth), S (DNA replication), G2 (preparation for mitosis).

M Phase: Prophase, Metaphase, Anaphase, Telophase, and Cytokinesis.

Cyclins and Cdks: 

Cyclins activate Cyclin-dependent kinases (Cdks) to regulate the progression of the cell cycle.

G1/S-cyclin: Highest in G1 and initiates DNA replication.

S-cyclin: Highest in S-phase to ensure DNA replication.

M-cyclin: Highest in M-phase, facilitating mitosis.

Cell Cycle Regulatory Proteins:

CKIs (p27): Inhibit cyclin/Cdk activity to halt cell cycle progression.

Wee1: Kinase that inhibits cyclin/CDK activity.

Cdc25: Phosphatase that activates cyclin/CDKs.

APC/C: Ubiquitin ligase complex that targets proteins for degradation, regulating mitosis progression.

Centrosome Duplication, Cohesin, and Kinetochore:

Centrosomes duplicate during interphase to form the spindle apparatus in mitosis.

Cohesin holds sister chromatids together until anaphase.

The kinetochore attaches chromosomes to the mitotic spindle.

Chapter 18 - Cell Death

Apoptosis vs. Necrosis:

Apoptosis: Programmed cell death, a controlled process that eliminates unwanted cells without inflammation.

Necrosis: Uncontrolled cell death due to injury, leading to inflammation.

Intracellular vs. Extracellular Apoptotic Cascade:

Intracellular: Mitochondria release cytochrome C, activating caspases.

Extracellular: Death ligands like Fas or TNF bind to death receptors, activating caspases.

Caspases in Apoptosis:

Initiator Caspases: Caspases 8 and 9 start the apoptotic cascade.

Executioner Caspases: Caspases 3, 6, and 7 cleave key cellular proteins, leading to cell death.

Mitochondria in Apoptosis:

Mitochondrial outer membrane permeability is altered, leading to cytochrome C release, which forms the apoptosome (with Apaf1) that activates caspase-9.

Proteins and Processes in Apoptosis:

Bcl2: Regulates mitochondrial membrane integrity; pro-apoptotic and anti-apoptotic forms.

Phagocytes remove apoptotic cells by phagocytosis.

Chapter 19 - Cell Junctions and Extracellular Matrix

Types of Cell Junctions:

Tight Junctions: Seal gaps between adjacent cells, preventing leakage.

Adherens Junctions: Anchor cells to each other via cadherins and catenins.

Desmosomes: Provide mechanical strength via cadherins linking intermediate filaments.

Gap Junctions: Allow direct communication between cells through connexons.

Hemidesmosomes: Anchor cells to the extracellular matrix via integrins.

Role of Cadherins and Catenins:

Cadherins: Calcium-dependent adhesion molecules that mediate cell-to-cell junctions.

Catenins: Link cadherins to the cytoskeleton (mainly actin filaments).

Extracellular Matrix (ECM) Components:

Proteoglycans: Composed of glycosaminoglycans (GAGs), they support cell signaling and structure.

Fibrous Proteins: Mainly collagen, which provides structural integrity.

Glycoproteins: Integrins are key transmembrane receptors that connect cells to the ECM.

Integrins: Involved in adhesion, signaling, and structural support. They bind ECM components like fibronectin and laminin.

Terms to Know/Define:

These terms are largely related to structures, proteins, and molecules involved in cell processes such as the cell cycle, apoptosis, and ECM. Some key examples:

Cadherin: A protein involved in cell adhesion.

Cyclin-dependent kinase (Cdk): A protein kinase that regulates the cell cycle.

Caspase: Enzymes responsible for the execution of apoptosis.

Laminin: ECM protein involved in basal lamina structure.