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Transcript
Chapter 12 The Cell Cycle PowerPoint® Lecture Presentations for Biology Eighth Edition Neil Campbell and Jane Reece Lectures by Chris Romero, updated by Erin Barley with contributions from Joan Sharp Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Overview: The Key Roles of Cell Division • The continuity of life is based on the reproduction of cells, or cell division • In unicellular organisms, division of one cell reproduces the entire organism • Multicellular organisms depend on cell division for: – Development from a fertilized cell – Growth – Repair • Cell division is an integral part of the cell cycle, the life of a cell from formation to its own division Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Concept 12.1: Cell division results in genetically identical daughter cells • Mitosis = Most cell division results in somatic cells (nonreproductive cells) - two sets of chromosomes with identical genetic information, DNA • Meiosis = A special type of division produces nonidentical daughter cells (gametes; reproductive cells; sperm and egg cells) and have half as many chromosomes as somatic cells • Genome - all the DNA in a cell – can consist of a single DNA molecule (common in prokaryotic cells) – number of DNA molecules (common in eukaryotic cells) • DNA molecules in a cell are packaged into chromosomes • Eukaryotic chromosomes consist of chromatin, a complex of DNA and protein that condenses during cell division Fig. 12-4 0.5 µm Chromosomes Chromosome arm DNA molecules Chromosome duplication (including DNA synthesis) Centromere Sister chromatids Separation of sister chromatids Centromere Sister chromatids Phases of the Cell Cycle • The cell cycle consists of – Mitotic (M) phase – mitosis (division of the nucleus) and cytokinesis (division of the cytoplasm) – Interphase (cell growth and copying of chromosomes in preparation for cell division) • Interphase (about 90% of the cell cycle) can be divided into subphases: – G1 phase (“first gap”) – S phase (“synthesis”) – G2 phase (“second gap”) Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Fig. 12-5 G1 S (DNA synthesis) G2 Fig. 12-6 G2 of Interphase Centrosomes Chromatin (with centriole (duplicated) pairs) Prophase Early mitotic Aster Centromere spindle Nucleolus Nuclear Plasma envelope membrane Chromosome, consisting of two sister chromatids Metaphase Prometaphase Fragments Nonkinetochore of nuclear microtubules envelope Kinetochore Kinetochore microtubule Anaphase Cleavage furrow Metaphase plate Spindle Centrosome at one spindle pole Telophase and Cytokinesis Daughter chromosomes Nuclear envelope forming Nucleolus forming •Mitotic spindle - (apparatus of microtubules that controls Sister chromosome movement) include: chromatids Aster Centrosome Metaphase plate •Centrosome - microtubule organizing center •spindle microtubules •Asters - radial array of short microtubules that extends from each centrosome •Kinetochores - some spindle microtubules attach to chromosomes and move them Kinetochores Overlapping nonkinetochore microtubules Kinetochore microtubules •Nonkinetochores push against each other elongating the cell •Metaphase plate - midway point between the spindle’s two poles 0.5 µm •In animal cells, cytokinesis occurs by a process known as cleavage, forming a cleavage furrow. In plant cells, a cell plate forms during cytokinesis 100 µm Cleavage furrow Contractile ring of microfilaments Vesicles forming cell plate Wall of parent cell Cell plate 1 µm New cell wall Daughter cells (a) Cleavage of an animal cell (SEM) Daughter cells (b) Cell plate formation in a plant cell (TEM) Fig. 12-11-4 •Prokaryotes (bacteria and archaea) reproduce by cell division called binary fission •Chromosomes replicate (beginning at the origin of replication), and the two daughter chromosomes move apart Cell wall Origin of replication E. coli cell Two copies of origin Origin Plasma membrane Bacterial chromosome Origin Fig. 12-12 Bacterial chromosome (a) Bacteria Chromosomes Microtubules The Evolution of Intact nuclear envelope (b) Dinoflagellates Kinetochore microtubule Mitosis Intact nuclear envelope (c) Diatoms and yeasts Kinetochore microtubule Fragments of nuclear envelope (d) Most eukaryotes •Since prokaryotes evolved before eukaryotes, mitosis probably evolved from binary fission •Certain protists exhibit types of cell division that seem intermediate between binary fission and mitosis Fig. 12-14 Cell cycle control system is similar to a clock regulated by both internal and external controls G1 checkpoint Control system G1 M M checkpoint G2 G2 checkpoint S Fig. 12-15 G0 G1 checkpoint G1 G1 (a) Cell receives a go-ahead signal (b) Cell does not receive a go-ahead signal •G0 phase - a nondividing state The Cell Cycle Clock: Cyclins & Cyclin-Dependent Kinase • Two types of regulatory proteins are involved in cell cycle control: cyclins and cyclindependent kinases (Cdks) • The activity of cyclins and Cdks fluctuates during the cell cycle • MPF (maturation-promoting factor) is a cyclinCdk complex that triggers a cell’s passage past the G2 checkpoint into the M phase Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Fig. 12-17 M S G1 G2 M G1 S G2 M G1 MPF activity Cyclin concentration Time (a) Fluctuation of MPF activity and cyclin concentration during the cell cycle Degraded cyclin G2 checkpoint Cyclin is degraded MPF Cdk Cyclin (b) Molecular mechanisms that help regulate the cell cycle Cyclin accumulation Cdk Stop and Go Signs: Internal and External Signals at the Checkpoints • Internal signal examples – kinetochores not attached to spindle microtubules send a signal that delays anaphase • Some external signals are growth factors, proteins released by certain cells that stimulate other cells to divide • For example, platelet-derived growth factor (PDGF) stimulates the division of human fibroblast cells in culture Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Fig. 12-18 Scalpels Petri plate Without PDGF cells fail to divide With PDGF cells proliferate Cultured fibroblasts 10 µm Fig. 12-19 •Density-dependent inhibition - crowded cells stop dividing Anchorage dependence Density-dependent inhibition Density-dependent inhibition •Anchorage dependence (found in most animals) - must be attached to a substratum in order to divide 25 µm 25 µm (a) Normal mammalian cells (b) Cancer cells Loss of Cell Cycle Controls in Cancer Cells • Cancer cells exhibit neither density- dependent inhibition nor anchorage dependence • Cancer cells do not respond normally to the body’s control mechanisms • Cancer cells may not need growth factors to grow and divide: – They may make their own growth factor – They may convey a growth factor’s signal without the presence of the growth factor – They may have an abnormal cell cycle control system Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings • A normal cell is converted to a cancerous cell by a process called transformation • Cancer cells form tumors- masses of abnormal cells within otherwise normal tissue – at the original site = benign tumor – Malignant tumors = invade surrounding tissues • Metastasize, exporting cancer cells to other parts of the body, where they may form secondary tumors Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Fig. 12-20 Lymph vessel Tumor Blood vessel Cancer cell Metastatic tumor Glandular tissue 1 A tumor grows from a single cancer cell. 2 Cancer cells invade neighboring tissue. 3 Cancer cells spread to other parts of the body. 4 Cancer cells may survive and establish a new tumor in another part of the body.