Transcript Chapter 9 How Cells Reproduce

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?
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)
Chromosomes
 Characteristic
number
 Orderly coiling
 DNA winds 2x
around histones to
make nucleosomes
 Centromere
 Kinetochore
Nuclear DNA
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
9.2 Cell Cycle
 Series of events
from one cell
division to the next
Interphase
 G1
– Growth/functional
S
– Synthesis of DNA
 G2
– Prepare for division
Mitosis and
C-some #
 Diploid
– 2n
– 2 of each type
9.3 Closer look
 Prophase
– C-somes visible
– Centrioles duplicate
– Nuclear envelope
– MT docks at
kinetochores
Metaphase
 Alignment of csomes between
spindle poles
Anaphase
 Sister chromatids
move to opposite
spindle poles by
motor proteins
Telophase
 C-somes reach poles
 Decondense
 Vesicles reform
envelope
9.4 Cytokinesis
 Animals
– Contractile ring
– Cleavage furrow
 Plants
– New fibers made before
prophase
– Vesicles from Golgi fuse and
deposit materials for cell plate
Identifying phases of Mitosis
Phase Determination
9.5 When Control is lost
 Cell cycle
checkpoints
– Proteins monitor
DNA structure
– Proteins monitor
proceeding phases
– Favorable
conditions?
– Kinases
– Growth factors
Architecture of control system
 Growth assessed at G1 checkpoint
 DNA replication success assessed at G2
 Mitosis assessed at M checkpoint
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
Tumor supressors
 Inhibit
 Prevent binding of
cyclins to CdKs
 Recessive
 Gene p53 – role in
G1 checkpoint,
checks for DNA
errors
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
– Repair or not
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.
Cancers
 4 characteristics
– Grow & divide abnormally
– Cytoplasm & membrane altered
– Weakened capacity for adhesion
– Lethal effects
Control of the cell cycle game
http://nobelprize.org/educational_games/medicine/2001/