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Lecture 3

Lecture 3- Cellular Bio II.docx

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Department
Biology
Course
BIO 141
Professor
Uzwiak
Semester
Fall

Description
Lecture 3: Cellular Biology II I. Nucleus: control center for cellular function; contains genetic material A. Number of nuclei 1. Most cells have a single nucleus 2. Large cells (those with a large amount of cytoplasm) have to be multinucleate 3. Red blood cells—only cell lacking a nucleus B. Structures 1. Nuclear envelope a. Double membrane—inner and outer i. Outermembrane is continuous with ER ii. Nuclear pores iii. Selectively permeable b. Perinuclear cisterna—fluid between membranes 2. Nucleoli a. No membrane b. Ribosomes subunits are assembled here i. Large in growing cells c. Associated with chromatin region associated with DNA coding for rRNA i. Nuclear organizing regions (DNA regions) 3. Chromatin—DNA + globular histone a. Nucleosome—fundamental unit of chromatin i. Units of eight wrapped by DNA molecule b. Chromosomes: prior to cell division, chromatin condenses to form chromosomes II. Cell Life Cycle The cell cycle includes all events from a cell’s formation until it divides. The cell cycle includes two major periods: interphase and cell division (mitosis). A. Interphase: from cell formation until cell division 1. Metabolic or growth phase: all non-replication activities 2. Preparation for division 3. Subphases: a. G1: growth phase with little cell division related activites i. Can last minutes to years (G ) 0 b. S: synthetic phase; DNA replicates c. G2: brief period of growth where enzymes and other proteins necessary for division are synthesized i. Very brief 4. DNA replication (Do not need to know molecular events) B. Cell Division 1. Mitosis and cytokinesis 2. Characteristics of mitosis a. Daughter cells (2) are identical to mother cell b. No gain or loss of genetic material c. Series of continuous events d. Lasts about two hours 3. Phases of mitosis a. Prophase i. Prior to the start of prophase, centrioles have replicated (two pairs) ii. Chromatin condenses to form chromosomes iii. Chromosomes already replicated and consist of two sister chromatids iv. Sister chromatids are connected by centromere v. Nuceoli disappear vi. Centriole pairs are rearranged to focal loci for mitotic spindles (microtubules) vii. Nuclear membrane disappears and spindles interact with chromosomes viii. Spindles attach to kinetochores (proteins on centromere) ix. Kinetochore microtubules pull chromatids to center of the cell b. Metaphase i. Chromosomes cluster at the middle of the cell ii. Metaphase plate c. Anaphase i. Centromeres of the chromosomes split ii. Each chromatid is now a chromosome iii. Kinetochore fibers contract and pull chromosomes towards poles iii. Poles of cells are pushed apart to elongate the cell iv. V-shaped v. Shortest stage; minutes d. Telophase i. Chromosome movement stops ii. Chromosomes uncoil to form chromatin iii. Nuclear membrane reforms iv. Nucleoli reform v. Spindles disassemble 4. Cytokinesis—peripheral microfilaments contract at the cleavage furrow to squeeze the cells apart C. Meiosis (Chapter 28): gamete production; two consecutive divisions produce four daughter cells each with half as many chromosomes as mother cell 1. Nuclear divisions: Meiosis I and meiosis II 2. Meiosis I (preceded by interphase where DNA is replicated): Reduction Division a. Prophase I i. Chromosome form, nuclear membrane and nucleolus disappear ii. Synapsis: homologous chromosomes form tetrads; crossover points form (chiasmata) b. Metaphase I i. Tetrads align on equatorial plate c. Anaphase I i. Centromeres do not break (sister chromotids remain paired) ii. Homologous chromosomes separate, breaking at crossover points (exchange parts of chromosomes) iii. Paternal and maternal chromosomes are separated d. Telophase I i. Same events as telophase of mitosis ii. Cytokinesis follows iii. Daughter cells are haploid (Diploid amount of DNA but haploid chromosomal number) 3. Meiosis II (Like mitosis without DNA replication during interphase) a. Four daughter cells are produced each genetically unique from original mother cells III. Cancer Terms: A. Neoplasia—increase in new cells 1. Dystrophy—disorder arising from abnormal change in cell size a. Hypertrophy—increase in size of cells 2. Dyplasia—disorder arising from abnormal change in cell number a. Hyperplasia—increase in number of cells b. Aplasia—decrease in cell number i. Normal during development ii. Occurs later in life (e.g., dementias, osteoporosis) B. Tumor—unchecked growth of genetically abnormal cells 1. Classification based on characteristics a. Benign i. Looks like normal tissue ii. Grows slowly iii. Does not invade b. Malignant: Cancer i. Poorly differentiated ii. Grow fast iii. Invasive iv. Metastasize 2. Classification based on origin a. Carcinomas—epithelial origin i. Glandular ii. Squamous iii. Melanocyte b. Sarcomas—connective tissue origin i. Cartilage ii. Bone iii. Fibrous connective iv. Meninges 3. Classification based on prognosis or therapy a. Tumor mass b. Lymph involvement c. Metastasis C. Epidemiology—cause of disease; factors that lead to cancer For a few rare situations, there are known genetic defects (e.g., retinoblastoma) or viral agents (e.g., Burkitt’s lymphoma). But for most other cancers, the specific cause is not known. A. Risk factors 1. Host factors a. Age b. Sex c. Psychological factors d. Genetic factors 2. Environmental and lifestyle factors a. Geographic location b. Nutrition c. Occupation i. Asbestos ii. Pesticides iii. Radiation d. Cigarette smoking D. Etiology 1. Cancer has no single cause. Its etiology is complex, requiring both: a. DNA damage b. Inadequate physiological defense or repair 2. Initiation of cancer—Neoplastic Transformation a. Arise from a single cell b. Cell suffers multiple transforming genetic mutations i. Mutations are either inherited or acquired 3. Acquired mutations a. Random events during DNA replication b. Induced by mutagens (carcinogens) 4. Initial DNA damage promotes accumulation of further damage a. Damage typically involves genes that normally: i. Induce cell proliferation or growth (proto- oncogenes) ii. Inhibit growth of damaged cells (tumor suppressor genes) E. Treatment 1. Surgery—resection of the tumor 2. Radiation therapy—x-rays or gamma rays delivered to the tumor; induce apoptosis in radiosensitive cells (including normal cells) 3. Chemotherapy (antineoplastic agents)—cytotoxic drugs that induce DNA damage; normal cells are often better at repair and less vulnerable to apoptosis 4. Bone marrow transplantation—certain cancers require high doses of radiation or chemotherapy; such treatment is toxic to bone marrow 5. Biological response modifiers—agents that boost immune system response or antagonize tumor growth through other biological effects (e.g., interferon, cytokines, etc.) 6. Gene therapy—modify gene function; include synthetic nucleotide strands to repair DNA, antisense strands to prevent gene expression, insertion of gene sequences to produce normal gene products End Cell Biology
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