BIOL 113 Exam 2 Flashcards
(139 cards)
1
Q
what makes the primary structure (amino acid chain) of proteins?
A
ribosomes
2
Q
what are the features that sort proteins in order to ensure they end up in the same location?
A
signal sequence & chemical labels
3
Q
signal sequence
A
either the first few amino acids or the last few in the chain (part of the primary structure)
4
Q
chemical label
A
chemical group added to a protein after it’s finished being manufactured, folded, and specialized
5
Q
where does all amino acid manufacturing begin?
A
cytoplasm
6
Q
proteins with no signal and no chemical label
A
protein stays in cytoplasm and functions there
7
Q
proteins where the last few amino acids act as a signal
A
nucleus, peroxisome, mitochondria/chloroplast
8
Q
how are amino acids destined to leave the cytoplasm treated?
A
the first few amino acids serves as an ER signal
9
Q
endomembrane system
A
endoplasmic reticulum - golgi apparatus - lysosome
10
Q
what happens to proteins without a chemical label but an er signal?
A
go to the cell membrane to be embedded or leave the cell
11
Q
what happens to proteins with an er signal and chemical label?
A
sorted into vesicles that will deliver them to the ER or GA
12
Q
or each of the proteins listed below, which features must they
receive during their manufacture to be transported to the destination
in which they will function? (select all)
1. Enzyme catalase: functions in the
peroxisome.
2. Sodium/potassium pump: functions
embedded in the cell membrane.
3. Enzyme sulfatases: functions in the
lysosome.
4. Protein insulin: functions outside the cell.
A
1) Peroxisome signal
2) ER Signal
3) ER Sgnal & Chemical label
4) ER Signal
13
Q
The enzyme catalase functions in the peroxisome. The last three amino acids
in it’s chain are serine-lysine-leucine. This sequence serves as the peroxisome
signal.
1. During it’s manufacture, where is catalase’s primary structure completed?
a) In the cytoplasm
b) In the RER
c) In the peroxisome
d) In the ribosome
2. Where is catalase’s secondary and tertiary “folding” structure completed?
a) In the cytoplasm
b) In the RER
c) In the peroxisome
d) In the ribosome
A
1) A
2) A
14
Q
the primary structure of all proteins is made by ____ located in _____ (which is dictated by ___)
A
ribosomes; different areas; where the protein will be function
15
Q
A
16
Q
endomembrane system
A
series of 3 organells that are all continuous
17
Q
endoplasmic retuculum
A
formed from invaginations of the nuclear envelope, proteins travel through the RER and then bud off into vesicles
18
Q
Vesicles fuse to the _____ Proteins then leave to go to the ___ or bud off into vesicles that become ____
A
golgi apparatus, cell membrane, lysosomes
19
Q
- How does the RER and GA
physically connect to exchange
materials? - How does the GA and lysosome
physically connect to exchange
materials?
A
1) - Vesicles from the RER fuse to the Golgi Apparatus kind of like a bridge
2) - Vesicles bud off of the GA to become lysosomes
20
Q
White blood cells manufacture selectin proteins which they can
deploy outside the cell to recruit other white blood cells to the site
of an infection. Where would the selectin end up if there was a
defect in its ER signal?
a. The protein would be excreted from the cell
b. The protein would end up in the cytoplasm
c. The protein would end up in a vesicle in the cell
A
B -
21
Q
signal recognition particle
A
pauses translation
21
Q
where are proteins folded
A
endoplasmic reticulum
22
Q
glycoproteins
A
carbohydrate side chains bound to some proteins by enzymes
23
Q
- Immune cells like white blood cells, which manufacture lots of
proteins that must be secreted (like antibodies) by the cell.
a) Large and/or many golgi apparatuses
b) Small and/or few golgi apparatuses - Muscle cells, which make many proteins that function in the
mitochondria and rarely or never secrete any proteins.
a) Many ribosomes attached to the RER
b) Few ribosomes attached to the RER
A
- A - cell is making proteins that will be secreted/leave - they go through the endomembrane system (very pronounced EM system)
- B - Cell is making proteins that function inside mitochondria, proteins that function here are made by ribosomes in the cytoplasm - they don’t go to the RER
24
prokaryotic cells
unicellular organisms (bacteria). No membrane, no mitochondria, circular DNA, small
25
eukaryotic cells
multicellular organisms. Membranes, mitochondria, linear DNA in mult chromosomes, large size, desmasomes and plasmodesmata
26
1. Prokaryotic cells are not capable of protein synthesis.
2. Prokaryotic cells have DNA.
3. Eukaryotic cells can attach to other cells.
4. Eukaryotic cells are divided into compartments.
1. False
2. True
3. True
4. True
27
which organelles have their own ribosomes and DNA?
mitochondria and chloroplasts
28
theory of endosymbiosis
a bacteria got inside of an archaea cell and that bacteria evolved into the mitochondria and chloroplast
29
accepted mechanism of endosymbiosis
as Archean cell membrane folds inwards, enveloped a nearby bacteria via phagocytosis
30
newly proposed mechanism of endosymbiosis
rather than cell membrane folding inwards, protrusions grow outwards, and encircles cell, trapping bacteria inside the cell (like a double cell membrane)
31
why is asgard archaeon a good candidate to model mechanism B of endosymbiosis?
lacks any internal membranes or indications that it could phagocytose materials, has genes encoding proteins similar to those of eukaryotes, and sprouts tentacle-like protrusions.
32
The new evidence lends support for which
proposed mechanism?
The archaeal ancestor of eukaryotes likely had
a) The ability to do phagocytosis
b) Long projections
Therefore, the evidence suggests that the bacteria got
inside the proto-eukaryote cell through the process of
c) Engulfing the bacteria
d) Surrounding the bacteria
1) B*
2) D*
33
Regardless of mechanism, the notion that eukaryotes
evolved from an archaea that either engulfed or
surrounded a bacteria which evolved into the
mitochondria (or chloroplast) of eukaryotes is a
Theory
Therefore, the theory of endosymbiosis
a) Has an overwhelming amount of evidence
b) Has evidence but also some contradictions
c) Can never be amended
A*
34
1. Observational evidence demonstrates which of the following?
Choose all.
2. Experimental evidence demonstrates which of the following?
Choose all.
a. The ability of bacteria to infect prokaryotic cells.
b. The ability of invading bacteria and host cells to evolve symbiosis.
c. The similarity between mitochondria and chloroplasts with
bacteria.
d. The dissimilarity between mitochondria and chloroplasts with the
cell they operate in.
1) A, C *
2) B*
35
Eukaryotic cells are ___ than prokaryotic cells
larger
36
The increase in size ____ the surface area to volume ratio
decreases
37
increased size of cells have a ___ ability to take in nutrients and excrete waste when compared with smaller cells
decreased
38
Which of the following does compartmentalization cause?
a) Chemical reactions more efficient
b) Chemical reactions less efficient
c) Substrates sequestered together
d) Substrates all spread out in the cell
e) Enzymes all spread out in the cell.
f) Incompatible chemical reactions
separated.
A,C,F *
39
what are two common types of proteins that attach to each other?
those that compose the cell membrane and extracellular matrix
40
why do cells attach to each other?
temporarily to perform a function or semi-permanently to form a tissue
41
extracellular matrix
surrounds the outside of cell membrane and contains proteoglycans, collages, integrans
42
function of proteoglycans in ECM
protect cell (lots of carbs attached)
43
function pf collagen rope in ECM
provides strength and form
44
function of integrins in ECM
span the CM, connect the inside of cell to the ECM
45
what is the composition of the ECM?
unique to each cell type
46
When stomach cancer becomes metastatic the
cancer cells detach from the original tumor and travel solo in the blood
to invade other parts of the body. During this process, the extra
cellular matrix of the cancer cells also become detached. Therefore,
you would expect to see ____ in the cell membrane of metastatic
stomach cancer cells.
a) Excessive, robust proteoglycans.
b) Few, deformed proteoglycans.
c) Excessive, robust integrins.
d) Few, deformed integrins.
D **
47
Skin cells connect tightly to each other via
desmosomes: Integral membrane proteins that form bridges between
anchoring proteins that extend inside the cells.
1. Are these cells attaching temporarily to perform a function or
semi-permanently to form a tissue?
2. What would happen to skin if there was a mutation in one cell’s
desmosomes such that they could not connect to adjacent ones?
1. Semi-permanently to form a tissue
2. Skin tissue wouldn't form?**
48
Cell Communication
a signal sent to one cell has to recognize and bind to the correct recieving cell
49
signals
proteins or other molecules (hormones or neurotransmitter)
50
receptors
proteins on or inside the cell membrane of the receiving cells
51
How does a signal fit into a receptor?
perfectly
52
Identify: signal, sending cell, receptor and
receiving cell
Pancreas cells manufacture and secrete insulin, a protein hormone, into
the blood. Insulin encounters many cell types along the way. It only
binds to liver and skeletal muscle cells because those cells have an
insulin receptor embedded in their cell membranes. The binding of
insulin onto the receptor prompts the liver and skeletal muscle cells to recruit a protein that can transport glucose from the bloodstream into
the cells for use.
Signal: Insulin
Sending Cell: Pancreas cell
Receptor: Insulin receptor
Receiving Cell: Liver/Muscle cell**
53
Two potential outcomes of binding a signal to a receptor
- Regulate gene expression to cause a new protein to be made
- Activate/Inactivate a protein that already exists in the cell
54
1. Insulin is a lipid insoluble
hormone protein signal. It’s
receptor is
located___________.
Therefore, signal binding
causes__________.
2.Estrogen is lipid soluble. It’s
receptor is located_________.
Therefore, signal binding
causes_________.
a. On or embedded in the cell membrane.
b. Inside the cell.
c. Interacts with DNA directly to cause a new protein to be made.
d. Activates or inactivates a protein that already exists in the cell.
1) A, D
2) B, C ***
55
Signal Transduction
Conversion of an extracellular signal to an intracellular one (changes activity of proteins in a cell)
56
When a lipid ___ signal binds to a receptor it (in)/activates a protein that ____
insoluble; already exists in the cell
57
G-protein receptors
associated wth signal receptors that are embedded within the cell membrane - activity is regulated by a guanine nucleotide
58
When a G-protein is bound to GDP, it is ___
inactive
59
After the signaling molecule binds, what happens to the receptor to kick the gdp out from the G-protein
the receptor changes shape
60
what happens after the GDP is kicked off the G protein?
a GTP binds, triggering a change in the shape of the G protein, splitting it into two parts
61
Second messenger
a nonprotein molecule that elicits an intracellular response
62
what is so special about the signals impact on messenger(s)?
one signal can elicit many second messengers; this amplifies the original signal
63
When you are frightened, your nervous system
initiates the fight or flight response. As part of this
response, adrenaline is released in your bloodstream
and binds to a G Protein adrenaline receptor on your
muscle cells. The G protein signal transduction
pathway eventually results in activating glycogen
phosphorylase, the enzyme that breaks down
glycogen (a starch stored in muscles) into glucose.
The glucose is now available to be used by the
muscles for fighting or fleeing.
1. What is the signal?
2. What is the G protein receptor?
3. What is the enzyme?
4. What is the second messenger?
5. What is “triggers response”?
1. Adrenaline
2. Adrenaline receptor
3. Glycogen phosphorylase
4. GTP protein
5. Whatever frightened you***
64
When you are frightened, your nervous system initiates the fight or
flight response. As part of this response, adrenaline is released in your
bloodstream and binds to a G Protein adrenaline receptor on your
muscle cells. The G protein signal transduction pathway eventually
results in activating glycogen phosphorylase, the enzyme that breaks
down glycogen (a starch stored in muscles) into glucose. The glucose is
now available to be used by the muscles for fighting or fleeing.
1. If a mutation in the pathway’s associated
enzyme inhibits 2nd messenger generation,
which of the following would occur?
(Choose ALL)
a) adrenaline would bind to the receptor
b) GTP binds to G protein
c) active subunit binds to enzyme
d) second messenger is produced
e) have available glucose to fight or flee
2. If a mutation in glycogen phosphorylase
made it unable to be activated by the
second messenger, which of the following
would occur (Choose ALL)
a) adrenaline would bind to the receptor
b) GTP binds to G protein
c) active subunit binds to enzyme
d) second messenger is produced
e) have available glucose to fight or flee
1)a, b, c ***
2)a,b,c,d,e
65
what do RTK receptors do
transduce hormonal signals by catalyzing a reaction in the cell
66
DNA polymerase, the protein that catalyzes DNA synthesis, adds
nucleotides only to the 3’ end of the template strands....that means
that the daughter strand is always made in the:
a) 5’ to 3’ direction
b) 3’ to 5’ direction
A
67
why is the daughter strand made in the 5'-3' direction
because DNA polymerase copies in the 3'-5' direction
68
okazaki fragments
fragments of new daughter DNA
69
Would DNA ligase inhibition affect the
process of DNA synthesis?
a. Yes. Both the leading and lagging strands would not be synthesized
properly.
b. Yes. The lagging strand would not be synthesized properly.
c. No. Ligase is not necessary to bind Okazaki fragments together.
d. No. DNA polymerase can fix any mistakes caused by ligase inhibition.
B
70
proofreading
DNA polymerase can detect and remove an incorrect single base that it has added. Happens while the enzyme is working
71
mismatch repair
after DNA synthesis is complete - another set of proteins can identify mismatches, cut out a section, and DNA polymerase comes back to add the correct DNA, and ligase will come back to seal the breaks
72
Nucleotide excision repair
protein complexes detect damage and remove it, same as mismatch repair, but comes from damage caused by UV light
73
In the disease Xeroderma pigmentosum, there is a significant
increase in the risk of contracting skin cancer only. Which repair
system is faulty here?
a) Proofreading
b) Mismatch repair
c) Nucleotide excision repair
2. Stomach cancer can be caused by excessive alcohol consumption.
Often this damage is fixed by a repair system called methyl
transferase repair, which operates similarly to nucleotide excision
repair. In someone with stomach cancer caused by excessive alcohol
consumption which of the following is likely occurring?
a) Methyl transferase repair is not operating at all.
b) Methyl transfer repair is operating effectively.
1) C
2) A
74
Binary fission is a simple process, but mitosis is more
complicated as it involves multiple steps. Which features of
eukaryotes makes them unable to divide properly with a
process like binary fission and thus they require mitosis?
(select all)
Eukaryotes have...
a) membrane-bound nuclei.
b) different types of ribosomes.
c) many chromosomes, usually paired.
d) mitochondria.
C
75
G1 phase of interphase
DNA is uncondensed (chromatin). Cell is fulfilling its function
76
S phase of interphase
DNA replicates
77
G2 phase of interphase
the cell grows to prepare for M phase
78
Signaling molecule arrives and binds to RTK monomers, causing them to ____
dimerize
79
Dimerization activates RTK's ___ activity, which ____ RTK itself at _____ residues
kinase, phosphorylates, tyrosine
80
____ _____ bind to phosphorylated RTK. One of them activates Ras causing it to exchange ___ for ___
Bridging proteins, GDP, GTP
81
Activated _____ Triggers phosphorylation and activation of____ ______
protein kinases
82
_____ results, where each kinase phosphorylates a different kinase until a response is triggered in the cell
A phosphorylation cascade
83
what is the outcome of a phosphorylation cascade?
original signal is amplified
84
why is an RTK signal amplified after a phosphorylation cascade?
each copy catalyzes many more copies downstream, exponentially increasing the number of activated enzymes
85
in both G proteins and enzyme linked, what activates the enzyme?
addition of a phosphate group
86
why does phosphorylation activate enzymes?
phosphate attaches a negative charge to the surface of a protein, attracting or repelling chemical groups, which can change its' shape
87
Imagine that in a liver cell, Ras is defective and can not interact with GTP. Insulin
approaches the liver cell. What will occur (select ALL that apply)?
a) Insulin will bind.
b) Phosphorylation cascade.
c) Glucose transporter activated.
d) Glucose brought in from the bloodstream.
88
Noninsulin-dependent diabetes mellitus is a disease which results in abnormally high blood
sugar levels. The disease is caused by a defect in liver cell RTKs such that insulin can bind
to RTK, but RTK does not respond to that binding. In this disease, when insulin approaches
liver cells which of the following occurs? (select all)
a) RTK responds to insulin binding
b) RTK phosphorylates itself
c) Phosphorylation cascade is initiated
d) Glucose is taken in by the cell
e) None will occur
89
Noninsulin-dependent diabetes mellitus is a disease which results in abnormally high blood
sugar levels. The disease is caused by a defect in liver cell RTKs such that insulin can bind
to RTK, but RTK does not respond to that binding. In this disease, when insulin approaches
liver cells which of the following occurs? (select all)
a) RTK responds to insulin binding
b) RTK phosphorylates itself
c) Phosphorylation cascade is initiated
d) Glucose is taken in by the cell
e) None will occur
90
composition of nucleotides
phosphate group, nitrogenous base, deoxyribose/ribose sugar
91
differences between DNA and RNA
DNA: Nitrogenous bases of Cytosine, guanine, thymine, adenine
- Deoxyribose sugar
- Double stranded
RNA:
Nitrogenous bases of cytosine, guanine, uracil, adenine
- Ribose sugar
- Single stranded
92
RNA is more/less reactive than DNA because of the ____
more; extra OH group on 2' C
93
____ is transcribed into ____ which is read by a ______ to produce a ____
DNA, RNA, Ribosome, Protein
94
How is dna structured?
two strands are bound together in an antiparallel fashion, 3'-5' forming a double helix
95
What does 3' and 5' really mean?
5' end refers to the 5' C which attaches the phosphate to the sugar ()
96
antiparallel
when two nucleotides are bonded, they are arraned opposite in orientation to each other
97
How is DNA replicated?
Each strand is copied separately, each strand is separated and then the parental strands serve as a template for a new daughter strand
98
What is the result of DNA synthesis?
a. Two identical DNA double helices, each with one new
and one old strand.
b. Two identical DNA double helices, one with two new
strands and one with two old strands.
A***
99
replication bubble
forms during dna synthesis
100
replication fork
Y-shaped region where the parenta strands are separated, this is where active synthesis takes place
101
how do replication forks move relative to each other?
they move in opposite directions
102
_____ breaks hydrogen bonds between nucleotides and oepns the double helix so that the strands separate at ____
DNA helicase, the replication fork
103
what binds to relieve stress of the twisting force?
topoisomerase
104
what attaches to the separated strands to hold them open and prevent them from snapping back into a double helix?
single-stranded DNA-binding proteins
105
leading strand
strand synthesized towards the fork - straightforward synthesis
106
lagging strand
synthesized away from the fork - causes gaps in synthesis
107
how long is an RNA strand?
~ 10 nucleotides
108
_____ lays down primer on ___ strands
primase, both
109
why is a primer necessary?
DNA polymerase can only add nucleotides to a free OH group (can only extend a strand - when the strands are separated there are no free OH groups
110
Primer
small sequence of RNA providing the free 3' OH group
111
The decision
to divide is
made prior
to the
transition
from
A. G1 to S
B. S to G2
C. G2 to Mitosis
D. Mitosis to Cytokinesis
E. Cytokinesis to G
A
112
1. Imagine that
there is a mistake
during DNA
replication. During
which phase will
proofreading
operate to fix the
mistake?
2. If proofreading doesn’t fix the
mistake, when during the cell cycle is
the next time it can get fixed?
1. S phase of replication
2. G2 phase?
113
what phase does nucleus excision repair occur in?
G1
114
prophase
DNA condenses into compact chromosomes
115
spindle apparatus
microtubule proteins that move replicated chromosomes during early mitosis and pulls sister chromatids apart
116
prometaphase
nuclear envelope disintegrates. Kinesand and dynein motor proteins attach to the kinetochores at the centromere and walk it down the microtubles to the middle of the spindle
117
metaphase
the chromosomes are lined up at the metaphase plate - overlap in the middle of the cell STACKED UP AT THE METAPHASE PLATE
118
Anaphase
The cohesion that holds sister chromatids together splits - sister chromatids are pulled apart and homologous chromosomes end up together - the two poles of the spindle are pushed and pulled farther apart by specialized proteins
119
telophase
spindle microtubules are fully depolymerized to remove the spindle - sister chromatids reach the opposite poles and nuclear envelope re forms - two independed nuclei
120
cytokinesis
cytoplasm is divided equally between the two new regions to create new cells
121
In which phase would a cell get stuck if a mutation
caused...
1. Chromosomes begin to condense but do not complete condensation
2. Spindle fibers form but do not attach to kinetochores
3. Sister chromatids line up at the middle of the cell but do not separate from each other
4. Sister chromatids separate from each other but stop before reaching the poles
1. Prophase
2. Prometaphase
3. Anaphase
4. Telophase
122
1. Intestinal cells go through two cell cycles
per day. Which of the phase(s) do you think
is significantly shortened to accomplish
this?
2. Nerve cells (almost) never divide. Which
phase are the cells (almost) always in?
1. G1
2. G1 --> becomes G0
123
regulator molecules
active at checkpoints, they prevent division of cells that are damaged
124
what are three outcomes of a cell failing to pass a checkpoint?
- stay in a resting state (G0)
- fix DNA damage
- undergo apoptosis
125
cancer cell
a cell that has dna damage causing it to divide uncontrollably
126
cyclins
named after the phase they are active are most active in, promprt the movement of cells from one phase into the next
127
how do cyclins work?
bind enzymes called cyclin dependent kinases, phosphorylate target proteins, amking them more or less active
128
what happens when a cyclin binds to cdks?
- cyclin activates cdk
- guides it to a specific set of proteins for phosphorylation
129
For example, G1/S cyclin binds Cdk and sends it to S
phase targets. What would happen to helicase if there
was not enough G1/S cyclin in the cell to bind to Cdk?
Primase Helicase Topoiso
merase
a) Helicase would be activated and would initiate DNA replication.
b) Helicase would not be activated and DNA replication would not occur.
B
130
M phase promoting factor
- Composed of Cdk and M cyclin
- When concentration is high, causes formation of MPF
- kinase subunit catalyzes phosphoruylation
- induces M phase in all eukaryotes
131
anaphase promoting complex/cyclosome
adds ubiquitin tags to proteins that need to be destroyed (kills proteins that may start mitosis again)
132
Regulator molecules: Anaphase-
promoting complex/cyclosome
1. APC/C adds a ubiquitin to M cyclin at the end of mitosis, this causes
a) The destruction of MPF
b) The activation of MPF
2. Separase is an enzyme. When bound to securin, separase is
inactive. APC/C adds a ubiquitin to securin. This causes (select all)
a) The destruction of securin
b) The activation of securin
c) The activation of separase
d) The destruction of separase
1) A
2) A & C
133
Cancer cells often contain incorrect numbers and/or sets of chromosomes. Which of the
following sets of mutations would directly lead to a tumor of lung cancer cells that all contain an
abnormal number of chromosomes?
a) Cyclin underexpression. Faulty G1 checkpoint.
b) Cyclin overexpression. Properly functioning G1 checkpoint.
c) APC/C inhibition. Faulty M2 checkpoint.
d) APC/C overactivation. Properly functioning M2 checkpoint.
C
134
Cdks, cyclins and the APC/C respond to cues
from inside and outside the cell. These cues
regulate their activity.
1. In a normally operating cell, the presence of hormonal growth
factors will
a) Increase the activity of Cdks and cyclin
b) Decrease the activity of Cdks and cyclin
2. In a normally operating cell, DNA damage will
c) Increase the activity of Cdks and cyclin
d) Decrease the activity of Cdks and cyclin
1) A
2) B
135
p53 tumor suppressor gene
136
Despite their differences, all cancers arise from cells in
which multiple cell-cycle regulators have failed.
Predict what would be present in a cancer cell:
1. Negative regulators (like P53 tumor suppressor) will be
mutated such that they are
a) Inactive
b) Overactive
2. Positive regulators (like cyclins) will be mutated such that
they are
a) Inactive
b) Overactive
1) A
2) B
137
Healthy cell:
1.Without the presence of
the growth factor binding
RTK, Ras is ___ and the cell
___. (select for each blank)
a) Inactivated
b) Overactivated
c) Doesn’t divide
d) Divides
138
