Cell Division
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Transcript Cell Division
Cell Division
“Omnis cellula e
cellula”
The Key Roles of Cell Division
• Essential for
perpetuation of life:
Reproduction of
unicellular forms
• Development,
Growth, & Repair of
multicellular forms
DNA – The Blue Prints for Life
• Genome – cell’s endowment of
DNA
• Chromatin DNA-protein
complex
• Chromosomes “colored
bodies” make it possible for 3
meters of DNA to fit in one
eukaryotic cell
• Chromosome # is species
specific
• Somatic cells vs gametes
• Sister chromatids duplicated
chromosomes
– Centromere
– Telomere
The Mitotic Cycle
• Interphase 90%
– G = Grow, normal fx.
1
– S = Synthesis of DNA
– G2 = Prepares for cell division
• Mitosis
– PMAT
• Cytokinesis –cell pinches in 2
– Animals: Cytoplasm side consists
of a ring of actin-myosin filaments
that move past each other causing
the ring to contract (drawstrings)
– Plants: Golgi Vesicles move to
middle of cell coalesce cell
plate
Interphase
• Nucleus is well defined in
a nuclear envelope
• DNA is in the form of
loosely packed chromatin
fibers
• Accounts for 90% of cell
cycle
• Cell grows and copies
DNA in preparation for
mitosis
• Chromatin fibers become
tightly coiled into discrete
chromosomes
• The nucleoli and nuclear
envelope begin to
disappear
• Each duplicated
chromosome appears as
two identical sister
chromatids joined
together
• Mitotic spindles begin to
form from microtubules
extending from
centrosomes
• Kinetochore forms at
centromere region
Prophase
Metaphase
• Centrosomes are at opposite poles of the cell
• Chromosomes convene at metaphase plate
• Kinetochores of the sister chromatids are attached to
microtubules coming from opposite poles of the cell.
Anaphase
• Paired centromeres of
each chromosome
separate, liberating the
sister chromatids from
each other
• Kinetochore microtubules
shorten – moving the
daughter chromosomes
to opposite poles of the
cell.
Telophase
• Daughter nuclei form at
the two poles of the cell
• Nuclear envelopes arise
from the fragments of the
parent cell’s nuclear
envelope and other
portions of the
endomembrane system
• Chromatin fibers of each
chromosome become
less coiled
• http://www.cellsalive.c
om/cell_cycle.htm
• http://www.cellsalive.c
om/mitosis.htm
Mitotic Spindle
• Chromosome movement
is controlled by mitotic
spindle
• Spindle arises from
centrosomes
• Kinetochore microtubules
depolymerize, moving
chromosomes throughout
mitosis
• Nonkinetochore
microtubules elongate
cell
Evolution of Mitosis
(page 225)
• Prokaryotes – daughter chromosomes
move apart ????
• Dinoflagellates – nuclear envelope
stays intact for chromosomes to attach;
microtubules pass through n.e.
reinforcing spatial orientation of
nucleus fission
• Diatoms – n.e. remains intact;
microtubules from a spindle w/i
nucleus separating the chromosomes
nucleus splits
• Eukaryotes – n.e. breaks down
spindle fibers form outside of
nucleus attach to kinetochore for
separation of sister chromatids
Regulation of the Cell
Cycle
• Cell Cycle Check points: G1, G2,
&M
• G1 checkpoint Most important; if
cell does not receive signal to go
ahead to S then cell will go into G0
(nondividing state: liver, neuron)
• Cell cycle is driven by specific
chemical signals present in
cytoplasm (not dominoes)
• Cyclin = protein that has fluctuating
levels during cell cycle;
synthesized during interphase
• Cdk’s- protein kinases that must
attach to cyclin to be activated
• MPF “maturation promoting factor”:
composed of Cdk & cyclin
complex; promotes mitosis by
phosphorylating various proteins
–
One indirect effect is the breakdown of its
own cyclin (off switch)
• Internal Signals:
• M phase checkpoint
Messages from
kinetochores ensures that
chromosomes are
properly attatched to the
spindle at metaphase.
Why?
• Protects against missing
chromosomes
• External Signals: Growth
factors must be present
to stimulate the growth of
cells (specific)
• Density dependent
inhibition – growth factors
and nutrients are
insufficient to stimulate
growth
• Anchorage dependence –
most animal cells must be
anchored to a substratum
to divide
• CANCER CELLS
EXHIBIT NEITHER OF
THESE!!!!!
Cell Cycle
Control
and Mutation
Controls in the Cell
Cycle
• Checkpoints exist in
the cell cycle
• Cell determines if cell is
ready to enter next part
of cell cycle
http://highered.mcgrawhill.com/olc/dl/120082/bio
34a.swf
What Is Cancer?
• Cancer begins when the proteins that regulate the cell
cycle don’t work, the cell divides uncontrollably
– Mutations can be inherited or induced by exposure to U.V.
radiation or carcinogens that damage DNA and chromosomes
Cancer: Uncontrolled cell growth
• Tumor
– Malignant vs benign
• Metastasis
• Types of cancer
– Carcinoma (epithelials)
• Melanoma (melanocytes)
– Sarcoma
(muscle/connective)
– Osteogenic (bone)
– Leukemia (blood forming
organs) ↑ WBC’s
– Lymphoma (lymphatic)
• Malignant cells trigger
angiogenesis
Mutations to Cell-Cycle
Control Genes
• Proto-oncogenes: Normal genes on many different
chromosomes regulate cell division
• When mutated, they become oncogenes
• Many organisms have proto-oncogenes, so many
organisms can develop cancer
Errors that cause cancer
•
p53 is a protein that functions to
block the cell cycle if the DNA is
damaged. If the damage is
severe this protein can cause
apoptosis (cell death).
1.
p53 levels are increased in
damaged cells. This allows
time to repair DNA by
blocking the cell cycle.
2.
A p53 mutation is the most
frequent mutation leading to
cancer.
•
p27 is a protein that binds to
cyclin and CdK blocking entry
into S phase. Recent research
(Nat. Med.3, 152 (97)) suggests
that breast cancer prognosis is
determined by p27 levels.
Reduced levels of p27 predict a
poor outcome for breast cancer
patients.
From Benign to Malignant
• Angiogenesis – growth
of blood cells caused
by secretions from
cancer cells
– Increases the blood
supply to cancer
cells: more oxygen
and nutrients
• Cancer cells can divide
more
• Tumors develop,
sometimes filling entire
organs
From Benign to
Malignant
• Contact inhibition in
normal cells prevents
them from dividing all
the time, which would
force the new cells to
pile up on each other
• Anchorage
dependence in normal
cells keeps the cells in
place
Multiple Hit Model
• Many changes, or hits, to
the cancer cell are
required for malignancy
• Mutations can be
inherited and/or can
stem from environmental
exposures
• Knowledge of cancer
risk factors is important
• Earlier detection and
treatment of cancer
greatly increase the odds
of survival
Detection Methods:
Biopsy
• Different cancers are
detected by different
methods, including high
protein production
possibly indicating a
tumor
• Biopsy, the surgical
removal of cells, tissue,
or fluid for analysis is
performed
• Under a microscope,
benign tumors appear
orderly and resemble
other cells in the same
tissue
• Malignant tumors do not
resemble normal tissue
5.6 Meiosis
•
•
•
•
Occurs within gonads (testes:ovaries)
Meiosis produces sex cells – gametes (sperm:egg)
Gametes have half the chromosomes (23) that somatic cells do (46)
Meiosis reduces the number of chromosomes by one-half
Meiosis
contributes
to Genetic
Variation
• There are millions of
possible combinations
of genes that each
parent can produce
because of:
– Random alignment
of homologous pairs
– Crossing over
– Random
Feritlization (70
trillion)
Birth = paused at prophase I
Puberty = finishes meiosis I
Fertilization = finishes meiosis
*somatic cells
*divide once diploid
*forms identical cells
http://highered.
mcgrawhill.com/sites/0
072437316/stu
dent_view0/ch
apter12/animat
ions.html#
*gametes
*divide twicehaploid
*forms different cells
(crossing over)
Conjoined Twins
http://www.youtube.com/watch?v=ZzZYKg
grB34&feature=fvsr
http://www.youtube.com/watch?v=XM82Hs
0LEpc