Cell Division - Rochester Community Schools

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Transcript Cell Division - Rochester Community Schools

Chapter 9
 I. Prokaryote Cell Division (Bacteria/Archaea)
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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 .
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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
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A. produces clones (daughter cells)
B. unicellular organisms : reproduction
C. Multicellular organisms :
1. asexual reproduction (budding)
2. growth
3. replacement
4. repair
 II. Meiosis
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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
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B. no supercoiling
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C. Most DNA available for transcription
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D. not visible under microscope
 II. Chromatid
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A. nucleosomes supercoiled into compact
‘arms’
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B. DNA packaged for transport not use
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C. condensed chromosomes visible
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 Constriction in center =
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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.
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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
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 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…
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chromatids
 (pro-metaphase)
 Nuclear envelope breaks down
 Microtubules attach to …
kinetochores
 Polar microtubules overlap at equator
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 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
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 Begins when chromatids reach poles
 Microtubules disassemble
 Nuclear envelope reforms
 Chromosomes
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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
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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
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inflexible
 support wall
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 Interphase – time spent between cell divisions
(90% of cell cycle)
 Mitosis – nuclear division
 Cytokinesis – cytoplasmic division
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 G1 – gap 1- cell grows ( max size based on..
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SA:V ratio)
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cell performs its function for the body
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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 =
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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
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cyclin causing MPF to revert to
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inactive CDK
 MPF contains a CDK that when activated by cyclin
what does it do?
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phosphorylates other proteins
 Growth Factors = proteins released by cells that
cause nearby cells to divide
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*example of cell – cell communication*
 PDGF released by platelets cause
Fibroblast(wound repair) cells to divide
 1) PDGF binds to receptor on Fibroblast
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 2) signal transduction pathway initiated
 3) cell passes G1 checkpoint and starts to divide
 Cell Division limited by:
1) Density-dependent Inhibition
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cells that are crowded stop dividing
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2) Anchorage dependency –
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cell must be anchored to extra-cellular
matrix of a tissue to divide.
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 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
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avoids apoptosis
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ignores regular cell cycle signals
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uncontrolled cell division
 Benign tumor : cells stay anchored
 Malignant tumor cells spread = cancer
 Metastasis = spread of cancer cells
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 Mutation of Check Point Genes
 Change in chromosome number/structure
 Abnormal/irregular cell membrane
lacks attachment proteins
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damaged signal/receptor proteins
 Secrete signal molecules that encourage blood
vessel growth
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 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
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