2. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings PowerPoint Lectures for Biology, Seventh Edition Neil Campbell and Jane Reece Lectures by Chris Romero Chapter 9 The Cell Cycle G1 - first gap S - DNA synthesis (replication) G2 - second gap M - mitosis

3. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings For reproduction – asexual reproduction one-celled organisms For growth – from fertilized egg to multi-celled organism For repair & renewal – replace cells that die from normal wear & tear or from injury Why do cells divide? amoeba

4. Chromosome duplication (including DNA synthesis) 0.5 µm Sister chromatids Separation of sister chromatids http://www.youtube.com/watch?NR=1&featu re=endscreen&v=gbSIBhFwQ4s

5. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Centrioles Cell division – in animal cells, pair of centrioles organize microtubules spindle fibers – guide chromosomes in mitosis

6. LE 12-6ca G 2 OF INTERPHASE PROPHASEPROMETAPHASE

7. LE 12-6da METAPHASEANAPHASE TELOPHASE AND CYTOKINESIS 10 µm

8. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Cytokinesis: A Closer Look Cytokinesis Divides the Cytoplasm In animal cells, cytokinesis occurs by a process known as cleavage First, a cleavage furrow appearscleavage furrow – cleavage furrow = shallow groove near the location of the old metaphase plate A contractile ring of actin microfilaments in association with myosin, a protein – (Actin and myosin are also involved in muscle contraction and other movement functions ) The contraction of the dividing cell's ring of microfilaments is like the pulling of drawstrings – The cell is pinched in two Cytokinesis in plant cells is different because plant cells have cell walls. There is no cleavage furrow ! During telophase, vesicles from the Golgi apparatus move along microtubules to the middle of the cell (where the cell plate was) and coalesce, producing the cell plate – Cell-wall construction materials are carried in the vesicles and are continually deposited until a complete cell wall forms between the two daughter cells see next photos.

9. LE 12-10 Nucleus Cell plate Chromosomes Nucleolus Chromatin condensing 10 µm Prophase. The chromatin is condensing. The nucleolus is beginning to disappear. Although not yet visible in the micrograph, the mitotic spindle is starting to form. Prometaphase. We now see discrete chromosomes; each consists of two identical sister chromatids. Later in prometaphase, the nuclear envelope will fragment. Metaphase. The spindle is complete, and the chromosomes, attached to microtubules at their kinetochores, are all at the metaphase plate. Anaphase. The chromatids of each chromosome have separated, and the daughter chromosomes are moving to the ends of the cell as their kinetochore micro- tubules shorten. Telophase. Daughter nuclei are forming. Meanwhile, cytokinesis has started: The cell plate, which will divide the cytoplasm in two, is growing toward the perimeter of the parent cell.

10. LE 12-11_3 Origin of replication Cell wall Plasma membrane Bacterial chromosome E. coli cell Two copies of origin Chromosome replication begins. Soon thereafter, one copy of the origin moves rapidly toward the other end of the cell. Replication continues. One copy of the origin is now at each end of the cell. Origin Replication finishes. The plasma membrane grows inward, and new cell wall is deposited. Two daughter cells result.

11. LE 12-14 G 1 checkpoint G1G1 S M M checkpoint G 2 checkpoint G2G2 Control system

12. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings For many cells, the G 1 checkpoint seems to be the most important one – depends on amount of cyclins present. If a cell receives a go-ahead signal at the G 1 checkpoint, it will usually complete the S, G 2, and M phases and divide If the cell does not receive the go-ahead signal, it will exit the cycle, switching into a nondividing state called the G 0 phase (neurons, heart cells) Problems in cyclin genes cause cells to divide continously. – CANCER!

13. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings The Cell Cycle Clock: Cyclins and Cyclin-Dependent Kinases Two types of regulatory proteins are involved in cell cycle control: cyclins and cyclin- dependent kinases (Cdks) The activity of cyclins and Cdks fluctuates during the cell cycle, what pushes the cell to the next phase. Cdk levels in the cell remain fairly stable, but each must bind the appropriate cyclin (whose levels fluctuate) in order to be activated. They add phosphate groups to a variety of protein substrates that control processes in the cell cycle as ALL Kinases do!phosphate groups

14. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Cancer & Cell Growth Cancer is essentially a failure of cell division control – unrestrained, uncontrolled cell growth What control is lost? – gene p53 plays a key role in G 1 /S restriction point p53 protein halts cell division if it detects damaged DNA ALL cancers have to shut down p53 activity

15. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Cancer cells exhibit neither density-dependent inhibition nor anchorage dependence http://www.youtube.com/watch?v=8nlfP03bdxo&feature=youtu.be

16. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Loss of Cell Cycle Controls in Cancer Cells Cancer cells do not respond normally to the body’s control mechanisms due to mutations, carcinogens (name some) Cancer cells form tumors, masses of abnormal cells within otherwise normal tissue If abnormal cells remain at the original site, the lump is called a benign tumor Malignant tumors invade surrounding tissues and can metastasize, exporting cancer cells to other parts of the body, where they may form secondary tumors

17. Linked to BRCA gene defect in some women Cancer cell Blood vessel Lymph vessel Tumor Glandular tissue Metastatic tumor A tumor grows from a single cancer cell. Cancer cells invade neighboring tissue. Cancer cells spread through lymph and blood vessels to other parts of the body. A small percentage of cancer cells may survive and establish a new tumor in another part of the body.

18. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Development of Cancer Cancer develops only after a cell experiences ~6 key mutations (“hits”) – unlimited growth turn on growth promoter genes – ignore checkpoints turn off tumor suppressor genes (p53) – escape apoptosis turn off suicide genes – immortality = unlimited divisions turn on chromosome maintenance genes – promotes blood vessel growth – angiogenesis http://www.youtube.com/watch?v=aKBZbxBnpGM http://www.youtube.com/watch?v=aKBZbxBnpGM turn on blood vessel growth genes – overcome anchor & density dependence turn off touch-sensor gene

19. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings onion root tip

20. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Lab on Mitosis: Minimum count of 150 cells Make a hypothesis and null hypothesis. You and your partner will each take a slide of onion root tip cells (already at stations) In one field you will look at each cell and mark what phase it is in. Your partner will then switch fields and mark the phases they see. Combine all totals and get the total amount of cells counted. Make a NEAT data chart and return to your seat with all that info! Run a chi square on data – individual or class????