1. Chapter 9 How Cells Reproduce  Start with 3 questions: –What kind of information guides inheritance? –How is the information copied in a parent cell before being passed to the daughter cell? –What kind of mechanisms actually parcel out info to daughter cells?

2. 9-1 Overview  Mitosis – nuclear division in somatic cells –Growth, replacing cells, tissue repair –Plants, animals, fungi, protists  Meiosis – formation of gametes/spores –Basis of sexual reproduction –Develop from germ cells  Prokaryotes? –Binary fission (p. 336)‏

3. Chromosomes  Characteristic number  Orderly coiling  DNA winds 2x around histones to make nucleosomes  Centromere  Kinetochore

4. one chromosome (one dispersed DNA molecule + proteins; not duplicated)‏ one chromosome (threadlike and now duplicated; two DNA molecules + proteins)‏ one chromosome (duplicated and also condensed tightly)‏ p.61 Nuclear DNA

5. 9.2 Cell Cycle  Series of events from one cell division to the next

6. Interphase  G1 –Growth/functional  S –Synthesis of DNA  G2 –Prepare for division

7. Mitosis and C-some #  Diploid –2n –2 of each type

8. 9.3 Closer look  Prophase –C-somes visible –Centrioles duplicate –Nuclear envelope –MT docks at kinetochores

9. Metaphase  Alignment of c- somes between spindle poles

10. Anaphase  Sister chromatids move to opposite spindle poles by motor proteins

11. Telophase  C-somes reach poles  Decondense  Vesicles reform envelope

12. 9.4 Cytokinesis  Animals –Contractile ring –Cleavage furrow  Plants –New fibers made before prophase –Vesicles from Golgi fuse and deposit materials for cell plate

13. Identifying phases of Mitosis Phase Determination

14. 9.5 When Control is lost  Cell cycle checkpoints –Proteins monitor DNA structure –Proteins monitor proceeding phases –Favorable conditions? –Kinases –Growth factors

15. Architecture of control system  Growth assessed at G1 checkpoint  DNA replication success assessed at G2  Mitosis assessed at M checkpoint

16. Molecular Mechanisms  Cyclin dependent protein kinases (Cdks)‏ –Cyclins – bind to Cdks, allow them to work as enzymes –G2 - MPF  Growth factors – stimulate –Usually everyone gets equal amounts –Specific cell surface receptors –Broad or specific

17. Tumor supressors  Inhibit  Prevent binding of cyclins to CdKs  Recessive  Gene p53 – role in G1 checkpoint, checks for DNA errors –Repair or not Figure 2: p53 re-enforces G1 and G2 cell cycle arrest after DNA damage through the cyclin-dependent kinase inhibitor p21WAF1/CIPI Mdm2 and Bax are other p53 transcriptional targets, with Mdm2 regulating p53 levels and Bax mediating apoptosis

18. Proto-oncogenes  Stimulate  Mutation = oncogene  Dominant  Changes in surface receptors Figure 2. A modified receptor. Under normal circumstances membrane-bound receptors require the binding of their ligand to be in an activated state. In contrast, receptors encoded by oncogenes do not require the regulatory step of ligand binding to be active.

19. Cancers  4 characteristics –Grow & divide abnormally –Cytoplasm & membrane altered –Weakened capacity for adhesion –Lethal effects

20. http://nobelprize.org/educational_games/medicine/2001/ Control of the cell cycle game