Cell Communication (College Board AP® Biology): Exam Questions

Homeostatic maintenance of optimal blood glucose levels has been intensively studied in vertebrate organisms. 

Pancreatic hormones regulate blood glucose levels. Identify TWO pancreatic hormones and describe the effect of each hormone on blood glucose levels.

For ONE of the hormones you identified in (a), identify ONE target cell and discuss the mechanism by which the hormone can alter activity in that target cell. Include in your discussion a description of reception, cellular transduction, and response. 

Compare the cell-signaling mechanisms of steroid hormones and protein hormones. 

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

Describe FOUR steps in the activation of the mother's specific immune response following exposure to a bacterial pathogen. Predict how the mother's immune response would differ upon a second exposure to the same bacterial pathogen a year later.

Predict the most likely consequence for a nursing infant who is exposed to an intestinal bacterial pathogen (e.g., Salmonella) to which the mother was exposed three months earlier. Justify your prediction.

Figure 1. Cellular response to infection by pathogenic bacteria

Some pathogenic bacteria enter cælls, 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.

CELL FRACTIONS CONTAINING DIFFERENT CELLULAR PROTEINS

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

Make a claim about how cleaving inactive caspase-1 results in activation of caspase-1. A student claims that preinfection production of inactive precursors shortens the response time of a cell to a bacterial infection. Provide ONE reason to support the student's claim.

A student claims that the NF-_KB protein is located in the cytoplasm until the protein is needed for transcription. Justify the student's claim with evidence. Identify TWO fractions where N-terminal gasdermin would be found in cells infected with pathogenic bacteria.

Describe the most likely effect of gasdermin pore formation on water balance in the cell in a hypotonic environment.

Polycystic kidney disease (PKD) is an inherited disease that causes water loss from the body and affects cell division in the kidneys. Because water movement across cell membranes is related to ion movement, scientists investigated the role of the Na⁺/K⁺ ATPase (also known as the sodium/potassium pump) in this disease. Ouabain, a steroid hormone, binds to the Na⁺/K⁺ ATPase in plasma membranes. Individuals with PKD have a genetic mutation that results in an increased binding of ouabain to the Na⁺/K⁺ ATPase. The scientists treated normal human kidney (NHK) cells and PKD cells with increasing concentrations of ouabain and measured the number of cells (Figure 1) and the activity of the Na⁺/K⁺ ATPase (Figure 2) after a period of time. The scientists hypothesized that a signal transduction pathway that includes the protein kinases MEK and ERK (Figure 3) may play a role in PKD symptoms.

Figure 3. Signal transduction pathway hypothesized to play a role in the increased number of PKD cells

Describe the characteristics of the plasma membrane that prevent simple diffusion of Na⁺ and K⁺ across the membrane. Explain why ATP is required for the activity of the Na⁺/K ⁺ ATPase.

Identify a dependent variable in the experiment represented in Figure 1. Justify the use of normal human kidney (NHK) cells as a control in the experiments. Justify the use of a range of ouabain concentrations in the experiment represented in Figure 1.

Based on the data shown in Figure 2, describe the relationship between the concentration of ouabain and the Na⁺/K⁺ ATPase activity both in normal human kidney (NHK) cells AND in PKD cells. The scientists determined that Na⁺/K⁺ ATPase activity in PKD cells treated with 1 pM ouabain is 150 units of ATP hydrolyzed/sec. Calculate the expected Na⁺/K⁺ ATPase activity (units/sec) in PKD cells treated with 10⁶ pM ouabain.

In a third experiment, the scientists added an inhibitor of phosphorylated MEK (pMEK) to the PKD cells exposed to 10⁴ pM ouabain. Based on Figure 3, predict the change in the relative ratio of ERK to pERK in ouabain-treated PKD cells with the inhibitor compared with ouabain-treated PKD cells without the inhibitor. Provide reasoning to justify your prediction. Using the data in Figure 1 AND the signal transduction pathway represented in Figure 3, explain how the concentration of cyclin proteins may increase in PKD cells treated with 10⁴ pM ouabain.

The binding of an extracellular ligand to a G protein-coupled receptor in the plasma membrane of a cell triggers intracellular signaling (Figure 1, A). After ligand binding, GTP replaces the GDP that is bound to Gsα, a subunit of the G protein (Figure 1, B). This causes Gsα to activate other cellular proteins, including adenylyl cyclase that converts ATP to cyclic AMP (cAMP). The cAMP activates protein kinases (Figure 1, C). In cells that line the small intestine, a cAMP-activated protein kinase causes further signaling that ultimately results in the secretion of chloride ions (Cl¯) from the cells. Under normal conditions, Gsα hydrolyzes GTP to GDP, thus inactivating adenylyl cyclase and stopping the signal (Figure 1, A).

Figure 1. Under normal conditions, ligand binding to a G protein-coupled receptor results in chloride ion transport from an intestinal cell

Individuals infected with the bacterium Vibrio cholerae experience severe loss of water from the body (dehydration). This is due to the effects of the bacterial cholera toxin that enters intestinal cells. Scientists studied the effects of cholera toxin on four samples of isolated intestinal cell membranes containing the G protein-related signal transduction components shown in Figure 1. GTP was added to samples II and IV only; cholera toxin was added to samples Ill and IV only. The scientists then measured the amount of cAMP produced by the adenylyl cyclase in each sample (Table 1).

TABLE 1. AMOUNT OF cAMP PRODUCED FROM INTESTINAL CELL MEMBRANES IN THE ABSENCE OR PRESENCE OF CHOLERA TOXIN

   present, +; absent, −

Describe one characteristic of a membrane that requires a channel be present for chloride ions to passively cross the membrane. Explain why the movement of chloride ions out of intestinal cells leads to water loss.

Identify an independent variable in the experiment. Identify a negative control in the experiment. Justify why the scientists included Sample Ill as a control treatment in the experiment.

Based on the data, describe the effect of cholera toxin on the synthesis of cAMP. Calculate the percent change in the rate of cAMP production due to the presence of cholera toxin in sample IV compared with sample II.

A drug is designed to bind to cholera toxin before it crosses the intestinal cell membrane. Scientists mix the drug with cholera toxin and then add this mixture and GTP to a sample of intestinal cell membranes. Predict the rate of cAMP production in pmol per mg adenylyl cyclase per min if the drug binds to all of the toxin. In a separate experiment, scientists engineer a mutant adenylyl cyclase that cannot be activated by Gsα. The scientists claim that cholera toxin will not cause excessive water loss from whole intestinal cells that contain the mutant adenylyl cyclase. Justify this claim.

ln eukaryotic microorganisms, the PHO signaling pathway regulates the expression of certain genes. These genes, Pho target genes, encode proteins involved in regulating phosphate homeostasis. When the level of extracellular inorganic phosphate (Pi) is high, a transcriptional activator Pho4 is phosphorylated by a complex of two proteins, Pho80—Pho85. As a result, the Pho target genes are not expressed. When the level of extracellular Pi is low, the activity of the Pho80—Pho85 complex is inhibited by another protein, Pho81, enabling Pho4 to induce the expression of these target genes. A simplified model of this pathway is shown in Figure 1.

Figure 1. A simplified model of the regulation of expression of Pho target genes in (A) a high-phosphate (high-Pi) environment and (B) a low-phosphate (low-Pi) environment

To study the role of the different proteins in the PHO pathway, researchers used a wild-type strain of yeast to create a strain with a mutant form of Pho81 (pho81mt) and a strain with a mutant form of Pho4 (pho4mt). In each of these mutant strains, researchers measured the activity of a particular enzyme, APase, which removes phosphates from its substrates and is encoded by PHO1, a Pho target gene (Table 1). They then determined the level of PHO1 mRNA relative to that of the wild-type yeast strain, which was set to 10.

TABLE 1. APase ACTIVITY AND RELATIVE AMOUNTS OF PHO1 mRNA IN WILD-TYPE AND MUTANT STRAINS OF YEAST IN HIGH- AND LOW-PHOSPHATE ENVIRONMENTS

Describe the effect that the addition of a charged phosphate group can have on a protein that would cause the protein to become inactive. Explain how a signal can be amplified during signal transduction in a pathway such as the PHO signaling pathway.

Based on Table 1', identify a dependent variable in the researchers' experiment: Justify the researchers" using the wild-type strain for the creation of the mutant strains. Justify the researchers' using mutant strains in which only a single component of the pathway was mutated in each strain.

Based on the data in Table 1 , identify the yeast strain and growth conditions that lead to the highest relative amount of PHO1 mRNA. Calculate the percent change in APase activity in wild-type yeast cells in a high-Pi environment compared with that of wild-type cells in a low-Pi environment.

In a follow-up experiment, researchers created a strain of yeast with a mutation that resulted in a nonfunctional Pho85 protein. Based on Figure 1, predict the effects of this mutation on PHO1 expression in the mutant strain in a high-Pi environment. Provide reasoning to justify your prediction.

Yeast (Saccharomyces cerevisiae) cells use signal transduction pathways to detect mating pheromones in their environment. The α-factor pheromone is secreted by α-cells and binds to receptor proteins on α-cells. This triggers a signal transduction cascade that leads to changes in gene expression and growth of a mating projection toward the α-cell.

A researcher designed an experiment to investigate the effect of continuous α-factor exposure on pathway activation and gene expression. Yeast α-cells were exposed to α-factor for different durations. The expression of a pathway target gene (FUS1) was measured using quantitative PCR, and the results are shown below.

Table 1: Expression of FUS1 gene after exposure to α-factor pheromone

(i) Describe the role of signal transduction in the yeast mating response.

(ii) Explain how ligand binding results in a change in gene expression.

(i) Identify one appropriate control that should be included in this experiment.

(ii) Describe one assumption the researcher must make when interpreting the results.

(i) Determine during which time interval the signal transduction pathway was most active.

(ii) Justify your answer using evidence from the data.

(i) Predict how the presence of a mutation that blocks negative feedback would affect FUS1 expression at 120 minutes.

(ii) Justify your prediction.

In mammals, blood glucose levels are regulated by the hormone insulin. Following a meal, insulin is released into the bloodstream, where it binds to receptors on liver cells. This activates phosphorylation cascades that stimulate translocation of glucose transporters to the cell membrane. In turn, enzymes catalyzing glycogen synthesis are activated. Insulin maintains homeostasis through negative feedback loops.

A researcher measured blood glucose concentration in a group of mice over 3 hours following a glucose-rich meal. Some mice were normal (wild-type), while others carried a mutation that blocks insulin receptor activation (insulin-resistant mice). The researcher's results are shown in the table below.

Table 1: Blood glucose concentration (mg/dL) in mice

(i) Describe the role of insulin in regulating blood glucose levels.

(ii) Explain how a signal transduction pathway allows insulin to produce a cellular response.

Construct a line graph showing the change in blood glucose concentration over time for both groups.

(i) Determine the effectiveness of glucose regulation in the two groups using the data in Table 1.

(ii) Use the concept of negative feedback to explain your analysis of the data in Table 1.

(i) Predict how insulin resistance would affect the ability of cells to carry out cellular respiration.

(ii) Justify your prediction based on the availability of glucose and the role of insulin.

Plants can detect pathogen-associated molecular patterns (PAMPs) using receptor proteins on the cell surface. Recognition of a PAMP activates a signal transduction pathway that leads to production of reactive oxygen species (ROS) and expression of defense-related genes. In many plants, salicylic acid (SA) is a hormone involved in amplifying the immune response through a positive feedback loop.

(i) Describe the role of receptor proteins in initiating a plant immune response.

(ii) Explain how a signal transduction pathway results in changes in gene expression.

A team of researchers investigates how exposure to a bacterial PAMP influences defense signaling in plants. They study two genotypes: wild-type plants and mutant plants lacking a receptor for salicylic acid (SA). Both are exposed to a PAMP. Six hours later, the team measures two markers of defense signaling:

• Hydrogen peroxide (H₂O₂), a reactive oxygen molecule produced during the early immune response.

• Expression of PR1, a gene associated with later stages of defense signaling.

The researchers collect three replicates per group and calculate the average response. Their results are shown in Figure 1.

(i) Explain why it is important to use multiple replicates when collecting data.

(ii) Explain the results shown in Figure 1.

(iii) Use the results to evaluate the role of SA signaling in regulating the immune response.

Explain how the data provide evidence for the role of a positive feedback loop in the plant immune response.

(i) Predict the effect on PR1 expression in a plant engineered to continuously produce SA, regardless of environmental signals.

(ii) Justify your prediction using the mechanism of positive feedback.

Ectothermic animals such as lizards rely on external temperatures to regulate body processes. Higher temperatures trigger conformational shape change in temperature-sensitive proteins, which initiates a cascade. This subsequently increases the expression of heat shock proteins (HSPs), which assist in the proper folding of other proteins, especially under stress conditions, without becoming part of the final protein structure. The production of HSPs is controlled by a signal transduction pathway that activates transcription of hsp genes when the temperature rises above a threshold.

A biologist investigates this pathway by exposing lizards to five temperatures (between 25°C and 45°C) and measuring HSP concentration and hsp70 gene expression after 4 hours.

Table 1: HSP concentration and hsp70 expression at different temperatures

Identify the trigger of this signal transduction pathway.

Identify the independent and dependent variables in this experiment.

The researcher claimed that once HSP levels are high enough, negative feedback inhibits further hsp 70 transcription to conserve resources.

Use evidence from the data to justify this claim.

If a lizard has a mutation in the heat shock factor (HSF) protein, it may fail to activate hsp gene transcription even when the temperature rises, leaving the cell without HSP protection.

Predict the effect of this on the organism.