1. Cell Division “ Omnis cellula e cellula ”

2. The Key Roles of Cell Division Essential for perpetuation of life: Reproduction of unicellular forms Development, Growth, & Repair of multicellular forms

3. DNA – The Blue Prints for Life Genome – cell’s endowment of DNA Chromatin  DNA-protein complex Chromosomes “colored bodies” make it possible for 3 meters of DNA to fit in one eukaryotic cell Chromosome # is species specific Somatic cells vs gametes Sister chromatids  duplicated chromosomes –Centromere –Telomere

4. The Mitotic Cycle Interphase  90% –G 1 = Grow, normal fx. –S = Synthesis of DNA –G 2 = Prepares for cell division Mitosis –PMAT Cytokinesis – cell pinches in 2 –Animals: Cytoplasm side consists of a ring of actin-myosin filaments that move past each other causing the ring to contract (drawstrings) –Plants: Golgi  Vesicles move to middle of cell  coalesce  cell plate

5. Interphase Nucleus is well defined in a nuclear envelope DNA is in the form of loosely packed chromatin fibers Accounts for 90% of cell cycle Cell grows and copies DNA in preparation for mitosis

6. Prophase Chromatin fibers become tightly coiled into discrete chromosomes The nucleoli and nuclear envelope begin to disappear Each duplicated chromosome appears as two identical sister chromatids joined together Mitotic spindles begin to form from microtubules extending from centrosomes Kinetochore forms at centromere region

7. Metaphase Centrosomes are at opposite poles of the cell Chromosomes convene at metaphase plate Kinetochores of the sister chromatids are attached to microtubules coming from opposite poles of the cell.

8. Anaphase Paired centromeres of each chromosome separate, liberating the sister chromatids from each other Kinetochore microtubules shorten – moving the daughter chromosomes to opposite poles of the cell.

9. Telophase Daughter nuclei form at the two poles of the cell Nuclear envelopes arise from the fragments of the parent cell’s nuclear envelope and other portions of the endomembrane system Chromatin fibers of each chromosome become less coiled

10. http://www.cellsalive.c om/cell_cycle.htmhttp://www.cellsalive.c om/cell_cycle.htm http://www.cellsalive.c om/mitosis.htmhttp://www.cellsalive.c om/mitosis.htm

11. Mitotic Spindle Chromosome movement is controlled by mitotic spindle Spindle arises from centrosomes Kinetochore microtubules depolymerize, moving chromosomes throughout mitosis Nonkinetochore microtubules elongate cell

12. Evolution of Mitosis (page 225) Prokaryotes – daughter chromosomes move apart  ???? Dinoflagellates – nuclear envelope stays intact for chromosomes to attach; microtubules pass through n.e. reinforcing spatial orientation of nucleus  fission Diatoms – n.e. remains intact; microtubules from a spindle w/i nucleus separating the chromosomes  nucleus splits Eukaryotes – n.e. breaks down  spindle fibers form outside of nucleus  attach to kinetochore for separation of sister chromatids

13. Regulation of the Cell Cycle Cell Cycle Check points: G1, G2, & M G1 checkpoint  Most important; if cell does not receive signal to go ahead to S then cell will go into G0 (nondividing state: liver, neuron) Cell cycle is driven by specific chemical signals present in cytoplasm (not dominoes) Cyclin = protein that has fluctuating levels during cell cycle; synthesized during interphase Cdk’s- protein kinases that must attach to cyclin to be activated MPF “maturation promoting factor”: composed of Cdk & cyclin complex; promotes mitosis by phosphorylating various proteins –One indirect effect is the breakdown of its own cyclin (off switch)

14. Internal Signals: M phase checkpoint Messages from kinetochores ensures that chromosomes are properly attatched to the spindle at metaphase. Why? Protects against missing chromosomes External Signals: Growth factors must be present to stimulate the growth of cells (specific) Density dependent inhibition – growth factors and nutrients are insufficient to stimulate growth Anchorage dependence – most animal cells must be anchored to a substratum to divide CANCER CELLS EXHIBIT NEITHER OF THESE!!!!!

15. Cell Cycle Control and Mutation Controls in the Cell Cycle Checkpoints exist in the cell cycle Cell determines if cell is ready to enter next part of cell cycle http://highered.mcgraw- hill.com/olc/dl/120082/bio 34a.swf

16. What Is Cancer? Cancer begins when the proteins that regulate the cell cycle don’t work, the cell divides uncontrollably –Mutations can be inherited or induced by exposure to U.V. radiation or carcinogens that damage DNA and chromosomes

17. Cancer: Uncontrolled cell growth Tumor –Malignant vs benign Metastasis Types of cancer –Carcinoma (epithelials) Melanoma (melanocytes) –Sarcoma (muscle/connective) –Osteogenic (bone) –Leukemia (blood forming organs) ↑ WBC’s –Lymphoma (lymphatic) Malignant cells trigger angiogenesis

18. Mutations to Cell-Cycle Control Genes Proto-oncogenes: Normal genes on many different chromosomes regulate cell division When mutated, they become oncogenes Many organisms have proto-oncogenes, so many organisms can develop cancer

21. Errors that cause cancer p53 is a protein that functions to block the cell cycle if the DNA is damaged. If the damage is severe this protein can cause apoptosis (cell death). 1.p53 levels are increased in damaged cells. This allows time to repair DNA by blocking the cell cycle. 2.A p53 mutation is the most frequent mutation leading to cancer. p27 is a protein that binds to cyclin and CdK blocking entry into S phase. Recent research (Nat. Med.3, 152 (97)) suggests that breast cancer prognosis is determined by p27 levels. Reduced levels of p27 predict a poor outcome for breast cancer patients.

22. From Benign to Malignant Angiogenesis – growth of blood cells caused by secretions from cancer cells –Increases the blood supply to cancer cells: more oxygen and nutrients Cancer cells can divide more Tumors develop, sometimes filling entire organs

23. From Benign to Malignant Contact inhibition in normal cells prevents them from dividing all the time, which would force the new cells to pile up on each other Anchorage dependence in normal cells keeps the cells in place

24. Multiple Hit Model Many changes, or hits, to the cancer cell are required for malignancy Mutations can be inherited and/or can stem from environmental exposures Knowledge of cancer risk factors is important Earlier detection and treatment of cancer greatly increase the odds of survival

25. Detection Methods: Biopsy Different cancers are detected by different methods, including high protein production possibly indicating a tumor Biopsy, the surgical removal of cells, tissue, or fluid for analysis is performed Under a microscope, benign tumors appear orderly and resemble other cells in the same tissue Malignant tumors do not resemble normal tissue

28. 5.6 Meiosis Occurs within gonads (testes:ovaries) Meiosis produces sex cells – gametes (sperm:egg) Gametes have half the chromosomes (23) that somatic cells do (46) Meiosis reduces the number of chromosomes by one-half

29. Meiosis contributes to Genetic Variation There are millions of possible combinations of genes that each parent can produce because of: –Random alignment of homologous pairs – Crossing over –Random Feritlization (70 trillion)

30. Birth = paused at prophase I Puberty = finishes meiosis I Fertilization = finishes meiosis

31. *somatic cells *divide once  diploid *forms identical cells *gametes *divide twice  haploid *forms different cells (crossing over) http://highered. mcgraw- hill.com/sites/0 072437316/stu dent_view0/ch apter12/animat ions.html#

32. Conjoined Twins http://www.youtube.com/watch?v=ZzZYKg grB34&feature=fvsr http://www.youtube.com/watch?v=XM82Hs 0LEpc