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AP Biology The Cell Cycle Part 1. One cell becoming two.

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Presentation on theme: "AP Biology The Cell Cycle Part 1. One cell becoming two."— Presentation transcript:

1 AP Biology The Cell Cycle Part 1

2 One cell becoming two

3 Binary Fission in Prokaryotes 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.

4 Chromatin vs. Chromosomes appearance within the cell.

5 Coiling up of Chromatin using histones

6 Somatic cells vs. Germ cells The egg surrounded by sperm.

7 Sister Chromatids

8 Mitosis (1 Division) vs. Meiosis (2 Divisions)

9 AP Biology The Cell Cycle Part 2

10 Centrioles

11

12 Interphase

13 Before and after the S phase

14 Interphase cell (Look at the chromatin in the blue nucleus and the yellow cytoskeleton.)

15 AP Biology Chapter 12: The Cell Cycle

16 Checkpoints (Is all going according to plan?)

17 . MPF activity G1G1 G2G2 S MS M G2G2 G1G1 M Cyclin Time Fluctuation of MPF activity and cyclin concentration during the cell cycle Relative concentration

18 . Degraded cyclin G 2 checkpoint S M G2G2 G1G1 Cdk Cyclin is degraded MPF Cyclin Cdk Molecular mechanisms that help regulate the cell cycle accumulation Cyclin

19 . Chromosome movement Microtubule Motor protein Chromosome Kinetochore Tubulin subunits

20 . Cells anchor to dish surface and divide (anchorage dependence). 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 gap and then stop (density-dependent inhibition). 25 µm Normal mammalian cells

21 . Cancer cells do not exhibit anchorage dependence or density-dependent inhibition. Cancer cells 25 µm

22 Malignant cancer cells from the breast (See the ABNORMAL “crab” shape of the cells.)

23 Mutations and Cancer Active form of p53 DNA DNA damage in genome UV light Protein kinases MUTATION Defective or missing transcription factor, such as p53, cannot activate transcription Protein kinases (phosphorylation cascade) Cell cycle-inhibiting pathway Cell cycle-stimulating pathway Protein that stimulates the cell cycle NUCLEUS DNA Gene expression Transcription factor (activator) Receptor G protein Growth factor MUTATION Hyperactive Ras protein (product of oncogene) issues signals on its own Protein that inhibits the cell cycle

24 AP Biology Cell Communication (Signaling) Part 1

25 Direct Contact

26 Local and Long Distance within an organism.

27 Phermones

28 Earl Sutherland

29 Step 1: Reception

30 Step 2: Transduction

31 Step 3: Response

32 See the CONFORMATION SHAPE CHANGE by the receptor protein caused by the ligand binding. Signal molecule (ligand) Gate closed Ions Ligand-gated ion channel receptor Plasma membrane Gate closed Gate open Cellular response

33 AP Biology Cell Communication (Signaling) Part 2

34 Phosphorylation and Hydrolysis

35 Receptor Protein

36 G protein Receptor

37 Tyrosine – Kinase Receptor

38 Ion Channel Receptors Signal molecule (ligand) Gate closed Ions Ligand-gated ion channel receptor Plasma membrane Gate closed Gate open Cellular response

39 Intracellular receptors

40 Secondary Messenger cAMP ATPCyclic AMPAMP Adenylyl cyclase Pyrophosphate PP i Phosphodiesterase H2OH2O

41 cAMP ATP Second messenger First messenger (signal molecule such as epinephrine) G-protein-linked receptor G protein Adenylyl cyclase Protein kinase A Cellular responses GTP

42 Secondary Messenger Calmodulin CYTOSOL Ca 2+ Endoplasmic reticulum (ER) IP 3 -gated calcium channel IP 3 (second messenger) DAG PIP 2 G-protein-linked receptor Phospholipase C G protein Signal molecule (first messenger) EXTRACELLULAR FLUID GTP Ca 2+ (second messenger) Various proteins activated Cellular re- sponses

43 AP Biology Cell Communication (Signaling) Part 3

44 Kinases “turn on” processes Phosphotases “turn off” processes

45 Small signal produces a BIG response

46 The Big picture Reception Growth factor Receptor Phosphorylation cascade Transduction CYTOPLASM Inactive transcription factor Active transcription factor P Response Gene mRNA DNA NUCLEUS

47 Scaffolding Proteins Signal molecule Plasma membrane Receptor Scaffolding protein Three different protein kinases

48 Tyrosine – Kinase Receptor (Evolution – Change over TIME)


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