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Honors Bio: Unit 6 Review Guide - Coggle Diagram
Honors Bio: Unit 6 Review Guide
Mitosis
How cells make copies of themselves
(nuclear division) 1-2 hours
Shortest phase of cell cycle
Helps cells grow and repair
Prophase: (chromosomes, condense ,spindle fibers form,
nuclear membrane & nucleolus disappear)
Metaphase: (chromosomes line up at the equator of the cell)
Anaphase: (sister chromatids separate)
Telophase: (nuclear membrane reforms, chromosomes unwind)
Cytokinesis: (cell division)
RESULT: 2 identical daughter cells
Vocab bank
centriole/centrosome = same thing (align at poles of cells)
Centromere = middle of chromosome where spindle fibers attach
Interphase
G0: The rest phase or quiesecent phase- cell does not grow or divide. Some
cells, like neurons, stay in this stage forever.
G1: In gap 1,the cell grows and gets ready
for chromosome duplication
S- This is the stage
when DNA replication occurs. Cells stay here until the cyclins and Cdk’s move
it to the G2 phase.
G2- In gap 2, DNA is duplicated and cell
Produces microtubules and other proteins needed for cell division
DNA replication
Occurs during S phase
DNA copying is necessary for organism growth
5 steps of DNA replication =
Helicase unwinds DNA by breaking hydrogen bonds between bases
DNA strands separate
DNA polymerase adds bases to growing strand (base pairs with original)
Reformation of hydrogen bonds between original and new strand
Ligase seals bonds beetween sugar-phosphate backbone
Mutations
Can happen during DNA replication
Can happen during G2 (chemicals, radiation, and uv rays = DNA damage)
Substitution occurs when one base is substituted for another base
• Deletion occurs when a base (or more) is missing from a gene
• Insertion occurs when an extra base (or more) are added to a gene
• Mistakes in tumor suppressor genes/ proto-oncogenes can result in cancer
Proto-oncogenes
Oncogenes = altered forms of protooncogenes
Responsible for promoting cell growth
When altered/mutated = become oncogenes and can promote tumor formation/growth
Mutations in proto-oncogenes are usually acquired.
½ copies mutated = change in cell growth and the formation of a tumor.
Dominant mutations
Tumor Suppresors
P53: p53- can activate DNA repair,hold the cell in G1 to repair cell, and
trigger apoptosis(cell death) if the cell is beyond repair.
normally present in our cells.
Control cell growth and cell death (apoptosis)
suppress tumor development
Both copies mutated = change in cell growth and tumor formation to occur
Recessive mutations
Can also be inherited [germline mutation where one copy of a tumor suppresor gene is inherited from parents and second one is acquired. If 2nd “hit”/mutation occurs in a cell where the tumor suppresor gene is needed to control cell growth = tumor formation due to two-hit theory]
Most of the genes associated with hereditary cancer are tumor suppressor genes. Nonetheless, most mutations in tumor suppressor genes are not inherited.
DNA repair genes
Mismatch-repair genes = DNA repair genes that correct naturally occurring spelling errors in the DNA.
When genes mutated = mistakes in DNA remain
If mistakes in tumor suppresors or protooncgenes = tumor formation + uncontrolled cell growth
can occur due to large doeses of radiation
Mutations in DNA repair genes can be inherited from a parent or acquired over time as the result of aging and environmental exposures.
Both members of gene pairs mutated = tumor formation
Recessive mutations
CDKs/Cyclins
Cell use cyclins and CD kinases to move from one phase to the next.
CD kinase levels are always the same; cyclin levels rise to push the cell into the next phase • Cancer cells either ignore cell signals, or receive wrong signals
• Certain genes, when mutated, can lead to cancer because their function affects the cell cycle
CdK= cyclin dependent kinase, and the levels are always the same
Cyclin levels rise and fall, depending on which cycle the cell is in
The CdK –cyclin complex = created at the beginning of a phase, and broken down towards the end of the phase, which is part of the signal for the cell to move on
These signals only allow the cell to move on if they have passed the checkpoints
If they have not, Cdk-cyclin levels can remain elevated and either the cell begins the process to destroy the cell Or in the case of cancer, the cell spins out of control
Cancer characteristics
Cancerous cells are smaller than normal cells, and cancerous cells move through the cell cycle faster
Cancer cells either ignore cell signals, or receive wrong signals
Certain genes, when mutated, can lead to cancer because their function affects the cell cycle
Cell cycle
The cell cycle- when cells grow, make proteins, and copy their DNA for mitosis as well as go through mitosis
Hayflick Limit
Cells can only divide 40-60 times
Telomeres shorten after each cell division, keeping track of the number of divisions.
Telomerase (enzyme) = responsible for fixing telomeres and is often overactive in cancer cells
Apoptosis
P53 is a transcription factor that binds DNA
When DNA is damaged, it can halt the cell cycle by using molecules to stop the cell from going further until the damage is fixed
If a cell can’t be fixed, p53 then tells the cell to start cell
death.
The cell is then shrunk down and broken into pieces
that a macrophage eats up and recycles for the cell
Example: formation of a baby’s fingers and toes
G1 Checkpoint- DNA and cell resources get checked by p53. Cells stay in
this phase until the G1 cyclin binds to a Cdk to move the cell to the next
phase.
G2 checkpoint- Cell has two things checked: DNA and proteins needed to
divide the cell. Many molecules check the DNA and proteins at this point.
M -The M stage is when nuclear
(chromosomes separate) and cytoplasmic (cytokinesis) division occur.
M checkpoint- MPF checks the spindles and chromosomes to make sure
that they are connected properly and ensures that the cell can successfully
complete mitosis.