Cell Division - Rochester Community Schools
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Transcript Cell Division - Rochester Community Schools
Chapter 9
I. Prokaryote Cell Division (Bacteria/Archaea)
A. No nucleus so no mitosis
B. No microtubules or motor proteins to
move chromosome.
C. Divide by Prokaryotic fission
1. single circular chromosome binds to
cell membrane
2. DNA replication in both directions
around circle
3. Cell divides by adding to cell membrane
II .
Eukaryotic Cell Division
A. DNA contained in nuclear membrane
B. DNA replicated prior to cell division
( in interphase)
C. Cell division divided into two parts
1. mitosis = division of nucleus
2. cytokinesis = division of cytoplasm
D. Microtubules and microfilaments needed
E. Motor proteins and ATP required
I. Mitosis
A. produces clones (daughter cells)
B. unicellular organisms : reproduction
C. Multicellular organisms :
1. asexual reproduction (budding)
2. growth
3. replacement
4. repair
II. Meiosis
A. produces haploid cells
1. chromosome number cut in ½
2. non-identical cells
3. gametes
B. only done for sexual reproduction
Somatic cell –
normal diploid body cell
Diploid cell –
has 2 copies of each
chromosome
Haploid cell –
has 1 copy of each
chromosome
Chromosome –
naturally occurring
segment of DNA and
associated proteins
I. Chromatin -
A. DNA wrapped around histones
B. no supercoiling
C. Most DNA available for transcription
D. not visible under microscope
II. Chromatid
A. nucleosomes supercoiled into compact
‘arms’
B. DNA packaged for transport not use
C. condensed chromosomes visible
Constriction in center =
centromere
= a region of DNA that binds to cohesin
proteins that function to hold sister
chromatids together
Other cohesins hold sister chromatids
together more loosely along their lengths
Identical
Formed by semi-conservative replication
While joined at centromere = 1 chromosome
unduplicated
duplicated
One chromosome
One chromosome
One chromatid
(one centromere)
One double helix
Two chromatids
Two double helixes
Genome = all of a cells DNA
All eukaryotes have set # Chromosome in their
genome
Humans have 46
Two of each type…
23 different types
1) Tubulin subunits in centrosome begin to
assemble into
microtubules.
http://www.youtube.com/watch?v=Rbbtbt2i8xA&list=PLCF9FC302EC1CA125
2) microtubules grow toward the center to form
spindle fibers
3) short microtubules form a radial array called
an aster
4) centrioles present in animals but not needed
Proteins located at centromere
Attachment site for some microtubules of
spindle
Polar microtubules overlap with
microtubules from opposite pole at center of
cell
Polar microtubules
Centrosomes begin producing microtubules &
moving toward opposite poles
Nucleoli disappear.
Chromosomes condense into…
chromatids
(pro-metaphase)
Nuclear envelope breaks down
Microtubules attach to …
kinetochores
Polar microtubules overlap at equator
Chromosomes lined up at equator
Pulled by kinetochore microtubules
C line up single file,
One sister chromatid on each side
Centrosomes reach poles
Cohesin proteins cleaved by
Separase enzymes
Separated sister chromatids move toward
opposite poles
Kinetochore microtubules shrink as they
depolymerize at centrosome
Motor proteins drag chromatids along
shrinking microtubules toward poles
Cell elongates as motor proteins push polar
microtubules past each other
Begins when chromatids reach poles
Microtubules disassemble
Nuclear envelope reforms
Chromosomes
de-condense into
chromatin
Cytokinesis begins before mitosis is complete
Different in plants and animals
Does not always take place
Contractile Ring Mechanism
1) a band of microfilaments of the cell cortex
contracts
2) indentation forms : cleavage furrow
3) ring contracts until cell membrane is
pinched in 2
Myosin motor proteins
Move actin filaments
Past each other to tighten
ring
Cell Plate Formation
Vesicles containing cell wall components move
from golgi to equator
Merging vesicle membranes form new cell
membrane
Cell wall components assembled in center of
merging vesicles form new primary cell wall
Primary cell wall : flexible stretchy allows growth
Secondary cell wall: deposited inside primary wall
solid
inflexible
support wall
Interphase – time spent between cell divisions
(90% of cell cycle)
Mitosis – nuclear division
Cytokinesis – cytoplasmic division
G1 – gap 1- cell grows ( max size based on..
SA:V ratio)
cell performs its function for the body
cell may never leave G1 (ex nerve cells)
S – synthesis :entire genome is synthesized
by semi-conservative replication
Growth and cell function continue
G2- gap 2 – cell grows & prepares to divide
duplicates centrosomes & centrioles (not
required: present in animals)
Controlled by activation of regulatory genes
These genes code for regulatory proteins.
Presence or Absence of these proteins
determine if a cell moves on to the next
phase of the cell cycle.
Cell cycle regulatory proteins are called
checkpoint proteins
The genes that code for these proteins are
checkpoint genes
Results from the failure of more than one
checkpoint gene
Which causes non-functional checkpoint
protein
Causes tumor development
May cause cancer
CDKs are a type of Kinase that only
functions when bound to cyclin.
Cyclins are a class of checkpoint protein that
activate enzymes by phosphorylation
Different versions of cyclin activate different
CDK enzymes
that are needed for the cell cycle to proceed
Table 1 Cell cycle regulators and cancer
Cyclin A 4 Complexed with CDK2 & 1 to regulate S phase
&G2–M Overexpressed in breast & hepatocellular carcinoma
Cyclin B1 Complexed with CDK1 to regulateG2–M
Overexpressed in some breast carcinoma
Cyclin D1 Complexed with CDK4/6 to regulate early G1
Overexpressed in multiple tumors
Cyclin D2 Complexed with CDK4/6 to regulate early G1
Overexpressed in some colorectal cancers
Cyclin E Complexed with CDK2 to regulate G1 & G1–S
transition Overexpressed in multiple tumors including
leukemias, carcinomas of the breast, colon, prostate
Inhibitors stop things
CKIs stop the CDK enzymes from working
Example:
CKI p21 stops CDK2 from working…thus
Stopping the transition from G1 – S phase
The CKI inhibitor molecule p21 is only active
when tumor suppressor gene p53 is
transcribed (copied) *** know p53 ***
M-phase Promoting Factor =
CDK-cyclin complex
High enough concentration of MPF allows
Cell to move from G2 into M phase
MPF concentration reduced in Anaphase by
breakdown of
cyclin causing MPF to revert to
inactive CDK
MPF contains a CDK that when activated by cyclin
what does it do?
phosphorylates other proteins
Growth Factors = proteins released by cells that
cause nearby cells to divide
*example of cell – cell communication*
PDGF released by platelets cause
Fibroblast(wound repair) cells to divide
1) PDGF binds to receptor on Fibroblast
2) signal transduction pathway initiated
3) cell passes G1 checkpoint and starts to divide
Cell Division limited by:
1) Density-dependent Inhibition
cells that are crowded stop dividing
2) Anchorage dependency –
cell must be anchored to extra-cellular
matrix of a tissue to divide.
Cancer Cells NOT inhibited by density or
anchorage
CC do NOT stop dividing when out of Growth
Factor
CC do not follow signals of check point genes
CC do not self-destruct by apoptosis
1 cell undergoes transformation
(damage to DNA)
Transformed cell avoids immune system
avoids apoptosis
ignores regular cell cycle signals
uncontrolled cell division
Benign tumor : cells stay anchored
Malignant tumor cells spread = cancer
Metastasis = spread of cancer cells
Mutation of Check Point Genes
Change in chromosome number/structure
Abnormal/irregular cell membrane
lacks attachment proteins
damaged signal/receptor proteins
Secrete signal molecules that encourage blood
vessel growth
Radiation for localized tumor
Chemotherapy – poisons most damaging to
dividing cells
1) G1 checkpoint – cycle initiation
a)controlled by cell size
b) growth factors
c) environment
2) G2 checkpoint – transition to M
a) DNA replication complete
b) DNA damage/mutations
3) M-spindle checkpoint
a) spindle attachment