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Summary Bio 310 Final Review Questions
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- Biology
Final Review Questions and Answers for Bio 310.
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Cell and Molec Final Review QuestionsWhat is a cell cycle "checkpoint"? How were they initially described experimentally?
Before the cell enters the next phase of the cell division cycle, it is to have somewhat of a
checklist to make sure DNA is properly replicated, conditions favorable, etc. Experimentally, they
were determined using yeast, mutagenizing them at least with one base pair, grow and isolate
them at 25 degrees celsius, and then go up to 30 degrees celsius to where cell cycle mutants
will have arrested development at different stages at different stages while under restrictive
temperature. Upon further experimentation, it was determined that checkpoints that stop
development like damaged DNA caused phosphorylation of p53 lead to expression of inhibitor
p21, stop CDK complex to prevent movement to the next cycle.
What is terminal differentiation and how is it different from G0?
G0 is the rest area, only during G1 in which they can re-enter the cell cycle when given
appropriate signals to do so and considered a proliferative state. Terminal differentiation will not
go back into the cell cycle to become a neuron-cell or alike that does not undergo cell-cycle
mechanisms.
Describe the DNA damage checkpoint to the cell cycle that involves p53.
p53 is involved in the first cell cycle checkpoint that occurs between the G1 and S phase. p53
acts as a transcriptional repressor because it will activate p21 which will act as an inhibitor for
the cyclin-CDK complex, which will then cause the Rb tumor suppressor gene to activate.
Describe how C. elegans could be used to look for genes involved in apoptosis:
C. elegans can be used to look for genes involved in apoptosis because these worms typically
develop approximately 1000 cells and kill off roughly 131 from birth to adulthood. The worms
can be mutagenized to develop extra cells which would be expected to have a mutation in the
gene necessary for apoptosis. [If the worm has more than ~1000 cells the cells that haven't died
but should have, have a mutation on a gene involved in apoptosis].
Compare and contrast necrosis and apoptosis
Apoptosis is caspase dependent cell death that is regulated with low permeability with no
immune reaction while necrosis is the high cell permeability or membrane disruption often dirty
causing inflammation/immune reaction that is uncontrolled and unregulated.
What is the intrinsic apoptotic pathway?
Intrinsic comes from mitochondria where BAX will poke holes into the mitochondrial membrane
and it will release cytochrome C where it can bind to adaptor protein in which multiple ones can
assemble into apoptosome which a procaspase9 can come in and be activated by the
,apoptosome promoting cleavage of pro-domain form of caspase9 which will activate caspase3,
leading to cell death as apoptosis being reliant on caspase.
What is the extrinsic apoptotic pathway?
FAS ligand from a killer T-cell will reach a FASR receptor and then the DISC complex will be
created of the cell undergoing apoptosis which will all eventually create a pro-domain cleavage
of FADD from initiator caspase8 on of which which are cysteine proteases that cleave the
backbone of aspartic acid residues that will eventually create caspase3, the executioner.
How did Kuida and colleagues determine that caspase-9 was involved in intrinsic pathway but
not an extrinsic pathway?
They knocked out cas9 gene in mice, which led to less apoptosis but still less survival as well as
brain enlargement which could indicate intrinsic apoptosis often important in
neurodevelopment. They also inhibited Cas9 with antibodies but that did not completely block
apoptosis with the extrinsic pathway in thymocytes still viable. Furthermore, with knockout
Cas9, the intrinsic apoptosis pathway can still be reconstituted with in vitro Cas9 and it did
based on radiolabeled cas3 being activated. Therefore, Cas-9 is involved with an intrinsic
pathway and not extrinsic.
You are at a pizza party and one of the guests says to you, "Oh, you are learning about cancer in
Bio 3220? Well, I've gotta tell you-- I think it's all a big shakedown. These researchers and
doctors have been trying to cure cancer for more than 50 years and there's still no cure for
cancer. What a rip off for good, hard working tax payers like myself!" How would you respond?
Cancer is practically impossible to cure since every reason for cancer is often different which
may include millions of different reasons as to why people get cancer and how often cancer
mutates in such a way that cannot easily be narrowed down to one cause let alone one
treatment method to attempt to fix it.
How is cervical cancer detected? Name the test and describe how it works.
You can detect cervical cancer through a test called Pap smear. This test works by taking a cell
sample at the surface of the cervix to be observed under a microscope. We can determine if
there is cervical cancer through the morphology of the epithelial cells. Normal cells will look big
and well defined, while cancerous cells will look small and have a small cytoplasm with a messy
morphology.
What are the ways in which oncogenes can be "activated"? How is chromatin remodeling
involved in cancer?
Oncogenes can be activated through mutations with or without in the DNA in various ways. A
mutation in the proto-oncogene will result in turning into an oncogene is one way. A nonmutant
, way can be amplification of the pro-oncogene where there are multiple copies of it and the
protein being overproduced. Chromatin remodeling is involved in cancer because of
chromosome rearrangement. Chromosome rearrangement is one of the ways in which
oncogenes can be activated because it creates new genes that can potentially function for
oncogenes.
What is the Knudsen or multi-hit hypothesis with respect to cancer?
The Knudsen or Multi - Hit Hypothesis explains that cancer is caused by the accumulation of
mutations within a cell. These mutations are in oncogenes that activate the genes that cause
cancer and mutations in tumor suppressor genes are required for cancer. Without these two
conditions, cancer cannot proliferate.
Describe >5 properties of cancer cells that make them different from normal cells
Cancer cells are small because their cell cycle is in overdrive, have mutations and their mutation
rates are higher, lack replication sequences (they can also regrow chromosome endings
meaning telomerase expression is higher), can leave their home tissue meaning they can be
metastatic (they use extracellular properties to do so and they under express Cadherins), have a
unique anaerobic metabolism, induce angiogenesis, lack contact inhibition, are resistant to
apoptosis and their cell division does not require attachment.
What is angiogenesis? How do tumors induce it?
Angiogenesis is the formation of new blood vessels and the process involves migration, growth,
and differentiation of endothelial cells which line blood vessel walls. Angiogenesis is induced
when tumors release VEGF and FGF. They release these chemicals because the tumor needs a
blood supply and oxygen to grow.
How can tumor initiating cell be identified? Describe the findings of Flavahan and colleagues for
brain tumor initiating cells.
They may include high GLUT3 (which has higher affinity than GLUT1) expression based on the
papers when studying glial cells, when studied, having higher aggressive phenotype when under
low glucose conditions with brain tumor initiator cells preferentially survive under low glucose
condition yet are efficient at high glucose intake which unironically somewhat inhibits their
aggressive behavior. Using shRNA to decrease expression of GLUT3 may make the initiator cells
less cancerous.
What is the innate immune system?
The immune system of which you are born with. They provide first line of defense against
microbes including the skin, mucous membranes, chemicals, secretions, white blood cells
(excluding lymphocytes) and complement proteins in that while microbes are recognized as
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