AP BIOLOGY Test Booklet

cell signal frq

1. Read each question carefully. Write your response in the space provided for each part of each question.
Answers must be written out in paragraph form. Outlines, bulleted lists, or diagrams alone are not
acceptable and will not be scored.

Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule binds to the wild-type
protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the
membrane protein and sometimes stimulate increased growth of blood vessels into the tumors.

Cells with a particular mutation in the gene ( cells) have much increased expression levels of
and stimulate greater growth of blood vessels than do cancer cells with the wild-type ( cells);
the cells with the mutant can trigger intracellular signaling in the absence of .

Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type
and is associated with phosphorylation and activation of kinase , expression of , and the ability of the
cancer cells to stimulate blood vessel growth.

Figure 1. A simplified model of the normal signaling pathway hypothesized to play a role in certain cancer cells
expressing and stimulating blood vessel growth into solid tumors

(a) Based on the signaling model shown in Figure 1, describe the role of molecule .

(b) Explain how the addition of a phosphate group to certain amino acids of likely affects the tertiary
structure and function of . Explain how the addition of a small could prevent the activation of kinase
. changes the shape of the structure>change its function;
mRNA will translate into protien, which affect D
(c) Based on the proposed signaling pathway, predict the relative amount of phosphorylated to unphosphorylated

unphosphorylated>phosphorylated; because the dinimish of transduction process>

unphsphorylated
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kinase in the cells when the cells are grown in nutrient broth lacking . Justify your prediction.

(d) Cells are treated with a compound that prevents the inactivation of kinase . Researchers claim that
cells treated with this compound will stimulate blood vessel-forming cell division to the same degree
as cells do in the absence of . Based on the information provided, provide reasoning to support
their claim.
一直处于激活的状态，血管扩张
both continuely active kinase D>espression of A>stimulates blood vessel(without B)
2. Acetylcholine receptor (AChR) proteins are found at the synapse between neurons and skeletal muscle cells.
Acetylcholine released from neurons binds to a specific site on the receptor proteins, which causes an ion channel
in the receptors to open and allow sodium ions (Na+) to enter muscle cells. The resulting depolarization of muscle
cells initiates muscle contractions. Another molecule, nicotine, can also bind to certain types of AChR proteins
and activate the receptors.

A researcher is investigating two different types of AChR proteins: type 1 and type 2. To determine which stimuli
activate the receptors, the researcher exposes muscle cells expressing the different types of receptor proteins to
stimuli and observes the results indicated in Table 1.

(a) Describe the difference in the structure AND function between AChR type 1 and AChR type 2.

(b) Acetylcholinesterase is an enzyme that breaks down acetylcholine in the synapse. Describe the effect of
inhibiting acetylcholinesterase on the muscle cells with AChR type 2.
钠离子通道打卡，肌肉收缩

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TABLE 1. SURVIVAL OF GENETICALLY MODIFIED B. THAILANDENSIS STRAINS

In bacterial communities, where resources are often limited, survival requires the ability to sense, respond to, and
cooperate or compete with neighboring organisms. In communities containing Burkholderia thailandensis bacteria, these
abilities rely in part on contact-dependent communication with neighboring cells. This communication involves a
signaling protein, protein S, that gets transported to the surface of the cell. When in direct physical contact with another
bacterial cell, protein S is cleaved and internalized by the recipient cell, where it can act as a nuclease. There are different
forms of protein S (e.g., S1, S2, S3) and different forms of an internal protein, protein R (e.g., R1, R2, R3). Recipient cells
are protected from the nuclease activity of protein S if they produce the appropriate form of protein R.

In an investigation, B. thailandensis strains were genetically engineered to produce different combinations of proteins S
and R. The cells were placed in a nutrient-deficient medium (T=0 hours) and cultured for 4 hours (T=4 hours). The
density of live cells in the culture was recorded at the two time points, T=0 hours and T=4 hours. The data are shown in
Table 1.

3. Explain the effect of expressing only S1 on the cells in culture 1. Describe the effect of expressing combinations
of protein S and protein R on the survival of the cells in culture 2 AND culture 3.

cells cannot survive; cell survival in culture 2 with S1 and R1, and cell cannot survivial in culture 3 with S1 and R3

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cell signal frq

4. Read each question carefully. Write your response in the space provided for each part of each question. Answers
must be written out in paragraph form. Outlines, bulleted lists, or diagrams alone are not acceptable and will not
be scored.

The compound eyes of arthropods contain photoreceptor cells surrounded by other cells such as cone cells and
pigment cells. Scientists studied how interactions between neighboring cells in the developing eyes of larval fruit
flies affect the differentiation of precursor cells that normally become the photoreceptors of adult wild-type
flies. One of their experiments is illustrated in Figure 1.

and cells are both present in a cluster of cells in the developing eye. cells have cell-surface proteins
called Boss. precursor cells have cell-surface receptor tyrosine kinases ( ) called and contain the
protein that is involved in intracellular signaling. are proteins with an extracellular portion that binds
to a ligand and an intracellular portion that transfers phosphate groups from to other proteins. Scientists
examined the fate of precursor cells in fly larvae with wild-type (normal) forms of the Boss, , and
proteins or in larvae with single mutations in the protein ( ) or double mutations in both ( )
and ( ). is a form of that is always active.

Figure 1. The fate of precursor cells in the presence of cells when the precursor cells are wild-type
(Wild Type) or have mutant proteins (Single Mutant) or have mutant and proteins (Double Mutant)

(a) Describe the first interaction that must occur between the precursor cell and the cell for the
precursor to differentiate to an photoreceptor cell. R8 boss and Sev RTK can bined together>activated Ras

(b) Describe how the defect in the Single-Mutant ( ) precursor cell causes the cell to become a cone cell
instead of a photoreceptor cell.
Boss cannot bind with Sev RTK> cannot actived Ras

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(c) The scientists predict that the presence of activated in the Double-Mutant ( ) precursor
cell will enable the cell to differentiate into an photoreceptor cell. Based on Figure 1, evaluate the likely
accuracy of their prediction. prediction is true; double mutate already activate Ras without combination of Boss
and Sev RTK
(d) The is expressed in more cell types than just precursor cells, and it appears to be important in
determining the phenotypes of these other cells. Explain how one receptor can induce different phenotypes in
different cell types. In different cell types, the pathway may be different

5.

The figure above represents a generalized hormone-signaling pathway. Briefly explain the role of each numbered
step in regulating target gene expression.

protein signal bind>receive

singal transuduct from plasma membrane to nucleus, initiate gene transduction>forming protein

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Figure 1. Cellular response to infection by pathogenic bacteria

Some pathogenic bacteria enter cells, replicate, and spread to other cells, causing illness in the host organism. Host cells
respond to these infections in a number of ways, one of which involves activating particular enzymatic pathways (Figure
1). Cells normally produce a steady supply of inactive caspase-1 protein. In response to intracellular pathogens, the
inactive caspase-1 is cleaved and forms an active caspase-1 (step 1). Active caspase-1 can cleave two other proteins.
When caspase-1 cleaves an inactive interleukin (step 2), the active portion of the interleukin is released from the cell. An
interleukin is a signaling molecule that can activate the immune response. When caspase-1 cleaves gasdermin (step 3), the
N-terminal portions of several gasdermin proteins associate in the cell membrane to form large, nonspecific pores.

Researchers created the model in Figure 1 using data from cell fractionation studies. In the experiments, various parts of
the cell were separated into fractions by mechanical and chemical methods. Specific proteins known to be located in
different parts of the cell were used as markers to determine the location of other proteins. The table below shows the
presence of known proteins in specific cellular fractions.

叶绿体
nucleus
lysosome
cell membrane

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6. Describe the effect of inhibiting step 3 on the formation of pores AND on the release of interleukin from the cell.

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cell signal frq

7. Read each question carefully. Write your response in the space provided for each part of each question.
Answers must be written out in paragraph form. Outlines, bulleted lists, or diagrams alone are not
acceptable and will not be scored.

Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule binds to the wild-type
protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the
membrane protein and sometimes stimulate increased growth of blood vessels into the tumors.

Cells with a particular mutation in the gene ( cells) have much increased expression levels of
and stimulate greater growth of blood vessels than do cancer cells with the wild-type ( cells);
the cells with the mutant can trigger intracellular signaling in the absence of .

Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type
and is associated with phosphorylation and activation of kinase , expression of , and the ability of the
cancer cells to stimulate blood vessel growth.

Figure 1. A simplified model of the normal signaling pathway hypothesized to play a role in certain cancer cells
expressing and stimulating blood vessel growth into solid tumors

(a) Based on the signaling model shown in Figure 1, describe the role of molecule in the activation of .

(b) Explain how a molecule such as kinase can amplify an extracellular signal. Explain how the mutant
protein is able to activate kinase even in the absence of its ligand.

(c) Based on the proposed signaling pathway, predict the relative activity of kinase in the cells
compared with kinase in the cells when both cell types are grown in nutrient broth lacking .
Justify your prediction.

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(d) The researchers claim that treatment with a compound that inhibits dephosphorylation of the intracellular
domain of the protein will inhibit expression of in cells but not in cells. Based
on the information provided, provide reasoning to refute their claim.

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cell signal frq

8. Read each question carefully. Write your response in the space provided for each part of each question.
Answers must be written out in paragraph form. Outlines, bulleted lists, or diagrams alone are not
acceptable and will not be scored.

Glycogen is a complex polymer of glucose molecules involved in the storage of energy in many organisms.
Depending on the signals received by a cell, different enzymes are activated, which will lead to either the
synthesis or breakdown of glycogen. The product of glycogen breakdown, glucose phosphate, can be modified
into glucose phosphate, an intermediate of glycolysis (Figure 1).

Figure 1. Glycogen synthesis and breakdown

In the liver, glycogen synthase and glycogen phosphorylase are regulated by kinases. These kinases transfer
phosphate groups from to amino acids in glycogen synthase and glycogen phosphorylase. Phosphorylase
kinase ( ) is a kinase that regulates glycogen synthase kinase ( ) activity. regulates the
activity of glycogen synthase. Phosphorylase kinase ( ) regulates the activity of glycogen phosphorylase. The
activity of these kinases depends on the activation of signaling pathways in response to the binding of specific cell
signals, including insulin and glucagon, to their receptors (Figure 2).

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Figure 2. A simplified model of signaling pathways in a liver cell that are activated by insulin and glucagon

(a) A cell where is always active has a mutation that results in the permanent activation of . Based
on the information in Figure 2, predict the effect of this mutation on the activity of glycogen synthase. Justify
your prediction.

(b) Describe the process that results in the activation of multiple copies of in response to the binding of a
single molecule of insulin to its receptor. Explain why insulin can stimulate the activation of but not the
activation of .

(c) Explain why an increase in glycogen phosphorylase activity might result in an increase in consumption in
the cell.

(d) A certain type of tumor results in the overproduction of glucagon. Researchers claim that treatment with
insulin can counteract the effects of the excess glucagon on the pathway shown in Figure 2. Provide reasoning to
justify the researchers' claim.

Strigolactones and karrikins are structurally similar compounds that can affect seed germination in certain species of
plants. However, plants with different life strategies (autotrophic plants or obligate parasitic weeds) germinate in response
to the presence of different compounds in the soil. After germination, many species of autotrophic plant release
strigolactones from their roots into the soil, which promotes uptake of nutrients. Figure 1. Effect of karrikins and
strigolactones on seed germination in an autotrophic host plant and its obligate parasitic weed

The graphs above represent the results of a laboratory experiment to test the effect of different concentrations of
strigolactones or karrikins on the seed germination of an autotrophic host plant and of an obligate parasitic weed.

9. A researcher proposes that the obligate parasitic weed requires exposure to a signal from the host plant before it
can germinate. Using the data as evidence, provide support for the researcher’s claim and give ONE reason the
response would be an advantage for the weed plants.

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