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Cell Cycle

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The complete explanation of cell cycle and it includes cell regulation, oncogenes, apoptosis, and characteristics of cancer.

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Cell Cycle

  1. 1. CELL CYCLE Muslima P. Liwalug MIB 1
  2. 2. OUTLINE:  Cell Cycle  Cell Regulation  Oncogenes  Apoptosis  Characteristics of Cancer
  3. 3. CELL CYCLE Simple Cell Cycle o Cell division in bacteria takes places in 2 stages • DNA is copied • Cell splits (binary fission) o Heredity in bacteria encoded in single circle of DNA Complex Cell Cycle o Eukaryotic DNA is contained in linear chromosomes • long DNA molecules packaged w/ proteins o Mitosis - Mechanism of cell division occurring in non-reproductive (somatic) cells o Meiosis - Mechanism of cell division occurring in reproductive (germ) cells
  4. 4. MITOSIS
  5. 5. A B C D
  6. 6. MEIOSIS
  7. 7. PROPHASE 1 1. Leptotene • Pairing. Homologous dyads (pairs of sister chromatids) • Thread-like chromatin with bead-like chromomeres • Plants- chrom drawn in 1 side of nucleus (synizesis) • Animals- drawn toward part of nuclear membrane close to centriole 2. Zygotene • The synaptinemal complex begins to form. • DNA strands of nonsister chromatids begin recombination. 3. Pachytene • Synapsis is now complete. • Recombination The steps in recombining DNA continue to the end of pachytene. • Crossing over involves chromatid breaks and repairs • Tetrad/bivalent formation occurs 4. Diplotene • DNA recombination is complete. • The synaptonemal complex begins to break down. • Coiled nature of chrom very apparent • The chromatids begin to pull apart ( terminalization) revealing chiasmata. 5. Diakinesis • Chrom assume unique configurations due to repulsion of chromatid pairs • This is followed by the chromosomes recondensing in preparation for metaphase I. • Bivalents bec distributed evenly in nucleus • Nucleolus disintegrates and spindle fibers form
  8. 8. MITOSIS MEIOSIS PARENT CELL (before chromosome replication) Site of crossing over MEIOSIS I PROPHASE I Tetrad formed by synapsis of homologous chromosomes PROPHASE Duplicated chromosome (two sister chromatids) METAPHASE Chromosome replication Chromosome replication 2n = 4 ANAPHASE TELOPHASE Chromosomes align at the metaphase plate Tetrads align at the metaphase plate METAPHASE I ANAPHASE I TELOPHASE I Sister chromatids separate during anaphase Homologous chromosomes separate during anaphase I; sister chromatids remain together No further chromosomal replication; sister chromatids separate during anaphase II 2n 2n Daughter cells of mitosis Daughter cells of meiosis II MEIOSIS II Daughter cells of meiosis I Haploid n = 2 n n n n MITOSIS VS. MEIOSIS
  9. 9. REGULATING THE CELL CYCLE
  10. 10. CELL CYCLE CHECK POINTS o Control loops that make initiation of one event dependent on the successful completion of an earlier event o Prevent damage that would ensue if cell were to undergo premature activity
  11. 11. CELL CYCLE CHECK POINTS o checkpoint for division ensures that the previous mitosis is finished o checkpoint for DNA integrity ensures that all DNA is replicated and that there is no damage to it o checkpoint for unreplicated DNA ensures that all DNA is replicated and replicated only once G1 checkpoint M checkpoint G2 checkpoint Control system
  12. 12. Growth factor Figure 8.8B Cell cycle control system Plasma membrane Receptor protein Signal transduction pathway G1 checkpoint Relay proteins THE BINDING OF GROWTH FACTORS TO SPECIFIC RECEPTORS ON THE PLASMA MEMBRANE IS USUALLY NECESSARY FOR CELL DIVISION
  13. 13. Control Mechanisms for cell division
  14. 14. Apoptosis – programmed cell death Schematic description of the controls in cell proliferation
  15. 15. Controlling the Cell Cycle • At critical points, further cell progress depends on a central set of switches regulated by cell feedback. – G1 – Cell growth assessed – G2 DNA replication assessed – M mitosis assessed • Gene p53 plays a key role in G1 checkpoint of cell division. – Gene’s product monitors integrity of DNA, checking for successful replication. • If protein detects damaged DNA, it halts cell division and stimulates repair enzymes. – Nonfunctional p53 genes allow cancer cells to repeatedly divide.
  16. 16. • Growth factors are proteins secreted by cells that stimulate other cells to divide After forming a single layer, cells have stopped dividing. Figure 8.8B Providing an additional supply of growth factors stimulates further cell division.
  17. 17. Anchorage, cell density, and chemical growth factors affect cell division In laboratory cultures, most normal cells divide only when attached to a surface – They are anchorage dependent Cells anchor to dish surface and divide. When cells have formed a complete single layer, they stop dividing (density- dependent inhibition). If some cells are scraped away, the remaining cells divide to fill the dish with a single layer and then stop (density- dependent inhibition). Cells continue dividing until they touch one another (Contact Inhibition) Growth factors are proteins secreted by cells that stimulate other cells to divide After forming a single layer, cells have stopped dividing. Providing an additional supply of growth factors stimulates further cell division.
  18. 18. FACTORS THAT CONTROL CELL DIVISION 1. cellular clock •determines the number of times the cell divides •dependent on cell type •ex. Connective tissue cells- higher rate of division than adult cells small intestine cells- divides during entire lifetime 2. Cellular inhibition -Normal cells in culture grow in a monolayer -When expanding monolayer encounters a barrier, it will grow around not over it -When surface of culture dish is covered with cells growth stops -Expression of orderly and limited cell growth 3. outside factors -hormones- cells lining uterus dependent on human progesterone Growth Factors 1. epidermal growth factor whenever there is injury to epidermis governed by contact inhibition also present in saliva-animals lick wounds 2. Platelet-derived growth factor - first identified to induce cell to divide in culture 4. intracellular factors -Early 1970s- subs + non-dividing cell - cell divides -Called it MPF- Maturation Promoting Factor -1988 (Lohka and Maller)- isolated MPF from Xenopus laevis -Induced cell to enter Mitosis (Called it M-Phase Promoting Factor)
  19. 19. Two Subunits of MPF 1. protein kinase-(p34 or cdc-2) o phosphorylates tyrosine and threonine o transfers phosphate groups from ATP to other proteins that mediate cell cycle 2. cyclin (p45) o -necessary for MPF to function o -undergoes a cyclic of synthesis and degradation o -control progression through cell cycle o -defective cyclin results in uncontrolled cell division→ parathyroid tumor, breast cancer and leukemia
  20. 20. PREVENTING THE PROLIFERATION OF CANCER CELLS  Tumor suppressor genes like p53 • Can arrest the cell cycle • Can launch the apoptotic pathway, causing the rogue cells to lyse A mutation in the p53 gene can lead to cancer  Immune cells (WBCs) such as NK cells can attack and lyse tumor cells • Some immune cells can signal the rogue cells to launch the apoptotic pathways
  21. 21. CANCER Genetic basis of cancer Genetic disease at the cellular level caused by an accumulation of mutations over a lifetime
  22. 22. WHAT CAUSE TUMOR GROWTH A. Proto-oncogenes  proteins involved in growth and cell-cell interactions B. Viruses  contain ONCOGENES (gene that promotes cancer)  Cancer genes which cause cell proliferation despite signal saying ‘STOP’  many cancers have no viral association  Insert into our chromosomes and transforms • Epstein-Barr Virus --> Burkitt’s Lymphoma • Papillomaviruses --> cervical cancer C. Tumor Suppressor Genes • Normal gene - prevents cells from dividing • when mutated - loss of function • cells divides out of control D. Loss of a cell´s ability to undergo apoptosis
  23. 23. o Tumors (neoplasms) • new cells are being produced in greater numbers than need • organization of the tissue becomes disrupted o Transformation • Process of converting a normal cell into malignant cell • rate of cell proliferation has increased
  24. 24. CHARACTERISTICS OF CANCER 1. Clonal in origin – a hallmark of cancer cell is that it divides to produce 2 daughter cells 2. Benign – non-invasive and precancerous genetic change 3. Malignant – when cells becomes cancerous and invasive to the neighboring cells - becomes metastatic (they can migrate to other parts of the body and cause secondary tumors)
  25. 25. CANCEROUS CELL o Has large and multiple nuclei o Irregular in shape o Cells overlapping neighboring cells o Loss of density – dependent or contact inhibition o Loss of anchorage dependence
  26. 26. DISTINCTIVE APPEARANCE OF CANCER CELLS
  27. 27. CERTAIN VIRUSES CAN CAUSE CANCER BY CARRYING VIRAL ONCOGENES INTO THE CELL o 15% of all human cancers are associated with viruses o Onco is incorporated into viral genome and this gene can become a viral oncogene Why does cancer occur when the gene is in viral genome? 1. Many copies of the virus made during viral replication may lead to overexpression of src gene 2. The incorporation of the src gene next to viral regulatory sequence may cause it to be overexpressed 3. The v-src gene may accumulate additional mutations that convert it to an oncogene
  28. 28. A GAIN-OF-FUNCTION MUTATION THAT PRODUCES AN ONCOGENE 1. The amount of the encoded protein is greatly increased 2. A change occurs in the structure of the encoded protein that causes it to be overly active 3. The encoded protein is expressed in a cell type where it is not normally expressed
  29. 29. GENETIC CHANGES IN PROTO-ONCOGENES CONVERT THEM TO ONCOGENES 1. Missense Mutation – changes of the structure of Ras protein can cause it to become permanently activated 2. Gene amplification – abnormal increase in the copy number of a proto-oncogene 3. Chromosomal translocation – translocation activates a proto-oncohgene Philadelphia chromosome - shortened arm of chromosome # 22

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