AP Biology 4

Thyroid-stimulating hormone (TSH) is a long-distance signaling molecule released by the anterior pituitary gland. Once released, TSH travels through the bloodstream to the thyroid gland, where it binds to G protein-coupled receptors called TSH receptors. This binding initiates signal transduction pathways that produce two thyroid hormones, T3 and T4. In individuals with hypothyroidism, TSH is released by the pituitary gland normally, but these individuals have consistently low levels of T3 and T4. Which of the following best explains why individuals with hypothyroidism have low levels of T3 and T4? - A mutation in their TSH receptors increases TSH recognition, resulting in decreased signal transduction. - A mutation in their TSH receptors decreases TSH recognition, resulting in decreased signal transduction. - A mutation in their TSH receptors increases TSH recognition, resulting in increased signal transduction. - A mutation in their TSH receptors decreases TSH recognition, resulting in increased signal transduction.

A mutation in their TSH receptors decreases TSH recognition, resulting in decreased signal transduction.

Which of the following best describes the cell communication occurring in the figure above? - A signal-emitting cell communicates with a far-away cell by releasing local regulators. - A signal-emitting cell communicates with a far-away cell by releasing long-distance signaling molecules. - A signal-emitting cell communicates with a nearby cell through direct cell-to-cell contact. - A signal-emitting cell communicates with a nearby cell by releasing local regulators.

A signal-emitting cell communicates with a nearby cell by releasing local regulators.

The information below shows and describes the initial steps of the MAPK/ERK signaling cascade. When epidermal growth factor (EGF) ligands bind to their receptors, the receptors pair up and act as kinases, attaching phosphate groups to one another's intracellular tails. The activated receptors then trigger a series of events that activate the kinase Raf. Which of the following toxins will most likely inhibit the activation of MEK? - A toxin that prevents the dephosphorylation activity of Raf - A toxin that prevents the kinase activity of Raf - A toxin that prevents MEK from phosphorylating Raf - A toxin that prevents the transfer of a phosphate group to Raf

A toxin that prevents the kinase activity of Raf

The information below shows and describes the intermediate steps of the MAPK/ERK signaling cascade. After MEK is activated, it phosphorylates and activates ERK. ERK goes on to phosphorylate and activate a variety of target molecules, including transcription factors like c-Myc that promote cell growth and division. Which of the following toxins will most likely inhibit the phosphorylation of c-Myc? - A toxin that prevents the dephosphorylation activity of MEK - A toxin that prevents the phosphorylation of ERK - A toxin that prevents the removal of a phosphate group from ERK - A toxin that prevents c-Myc from activating ERK

A toxin that prevents the phosphorylation of ERK

Acetylcholine is a neurotransmitter that helps control muscle contraction. This neurotransmitter functions differently depending on which type of muscle it interacts with. For example, acetylcholine promotes muscle contraction in skeletal muscle but inhibits contraction in heart muscle. Which of the following best explains why acetylcholine leads to different cellular responses in skeletal and heart muscle? - Acetylcholine binds to different types of receptors in skeletal and heart muscle. - Acetylcholine binds with less affinity to receptors in heart muscle than in skeletal muscle. - Acetylcholine binds more tightly to receptors in skeletal muscle than in heart muscle. - Acetylcholine binds to more receptors in skeletal muscle than in heart muscle.

Acetylcholine binds to different types of receptors in skeletal and heart muscle.

Which of the following mutated proteins is most likely to cause a cell to become cancerous? - An underactive version of a protein that promotes cell cycle progression - An underactive version of a protein that stimulates growth hormone receptors - An overactive version of a protein that promotes apoptosis - An overactive version of a protein that stimulates cell division

An overactive version of a protein that stimulates cell division

The image above depicts the signal transduction pathway of epinephrine. During one step in the pathway, the enzyme glycogen phosphorylase is phosphorylated, which activates the enzyme. If an inhibitor prevents glycogen phosphorylase from being activated during this pathway, which of the following will most likely occur? - Glycogen synthase will be activated in place of glycogen phosphorylase. - Blood glucose level will not increase in response to epinephrine. - Epinephrine will not bind to epinephrine receptor. - Glycogen levels will decrease in response to epinephrine.

Blood glucose level will not increase in response to epinephrine.

The diagram above depicts how the eukaryotic cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs). Based on the diagram, which of the following best describes the effect of a toxin that prevents the production of the G1cyclin? - DNA replication would be inhibited, causing the cell to stop dividing. - The mitotic cyclin would functionally replace G1 cyclin, allowing the cell to continue dividing normally. - The transition into mitosis would be blocked, causing the cell to stop dividing. - The cell cycle checkpoints would be ignored, causing the cell to become cancerous.

DNA replication would be inhibited, causing the cell to stop dividing.

The following excerpt and image come from a scientific paper written by Ebrahimi & Chess. They discuss the role of G proteins in olfaction, or the sense of smell. Each mammalian olfactory neuron appears to use the same machinery for transducing signals from its odorant receptor molecules. Upon odorant binding, the receptor is thought to activate Golf_\text{olf}​start subscript, start text, o, l, f, end text, end subscript, a G protein. Golf m_\text{olstart subscript, start text, o, l, f, end text, mediated activation of adenylate cyclase III then raises intracellular cAMP levels, causing a cyclic-nucleotide-gated channel to open. The influx of cations through this channel ultimately leads to the formation of an action potential, which allows the primary neuron to signal to the brain. A mutation in a component of this signal transduction pathway prevents the cyclic-nucleotide-gated channel from opening. Which of the following scientific questions would best help researchers understand how the mutation prevents the cyclic-nucleotide-gated channel from opening? - Does mutation cause the influx of cations into the cell? - Does mutation stimulate the conversion of ATP to cAMP? - Does the mutation block the activation of adenylate cyclase III? - Does mutation cause intracellular cAMP level to rise?

Does the mutation block the activation of adenylate cyclase III?

Adenoviruses are a family of highly contagious viruses that most commonly cause illnesses of the respiratory system, such as bronchitis or pneumonia. In the first phase of an adenovirus infection, the host cell expresses several viral proteins. One of these proteins, E1B-55k, inhibits the activity of the host protein p53, a tumor suppressor that arrests the cell cycle or induces apoptosis when DNA damage is detected. Which of the following claims is best supported by the information above? - E1B-55k causes infected cells to undergo programmed cell death. - E1B-55k decreases the likelihood of apoptosis in infected cells. - E1B-55k causes infected cells to transition out of the cell cycle and into the G0 phase. start subscript, 0, end subsc - E1B-55k increases the likelihood of cell cycle arrest in infected cells.

E1B-55k decreases the likelihood of apoptosis in infected cells.

The following is an excerpt from a scientific paper by Jean-Pierre Raufman. Cholera, an infectious disease that can kill humans within a matter of hours, is a manifestation of a highly efficient and specific toxin delivery mechanism. This mechanism, which is shared by several bacteria, delivers a potent toxin to activate selectively the adenylyl cyclase system of human intestinal secretory cells. This increases production of the ''second messenger'' cyclic adenosine monophosphate (cAMP) that activates an intestinal crypt cell chloride ion channel, thereby resulting in massive fluid and electrolyte secretion into the lumen of the gut. Raufman, J. P. (1998). Cholera. Am. J. Med. 104, 386-394. Based on the information above, which of the following is most likely to be observed in the intestinal environment of a person infected with cholera? - Elevated levels of intracellular ATP - Elevated levels of extracellular chloride ions - Reduced levels of extracellular chloride ions - Reduced levels of intracellular cAMP

Elevated levels of extracellular chloride ions

Enzymes often play a major role in signal transduction pathways. For example, enzymes can help convert an extracellular signal into an intracellular response. Specifically, adenylyl cyclase is an enzyme that catalyzes the conversion of ATP to cyclic AMP (cAMP). One competitive inhibitor of adenylyl cyclase is called MANT-ITP. Which of the following questions would best direct an investigation on how MANT-ITP impacts a signal transduction pathway? - How does MANT-ITP affect the shape of G protein-coupled receptors? - How does MANT-ITP affect the recognition of an extracellular signal? - How does MANT-ITP affect the response to intracellular signals? - How does MANT-ITP affect the binding of ligands to G protein-coupled receptors?

How does MANT-ITP affect the response to intracellular signals?

The endocrine system maintains homeostasis in the body through the release of various hormones. For example, the pancreas releases the hormone insulin to help regulate blood glucose homeostasis. Which of the following best describes the role of insulin in regulating blood glucose homeostasis? - Insulin is released in response to high blood glucose levels. This release triggers a positive feedback loop that further increases blood glucose levels. - Insulin is released in response to low blood glucose levels. This release triggers a negative feedback loop that returns blood glucose levels back to normal. - Insulin is released in response to high blood glucose levels. This release triggers a negative feedback loop that returns blood glucose levels back to normal. - Insulin is released in response to low blood glucose levels. This release triggers a positive feedback loop that further decreases blood glucose levels.

Insulin is released in response to high blood glucose levels. This release triggers a negative feedback loop that returns blood glucose levels back to normal.

Which of the following statements about feedback mechanisms is most accurate? - Positive feedback mechanisms maintain a system at its set point. - Positive feedback mechanisms bring a system closer to its set point. - Negative feedback mechanisms move a system further from its set point. - Negative feedback mechanisms return a system to its set point.

Negative feedback mechanisms return a system to its set point.

Which of the following correctly describes how positive and negative feedback are different? - Positive feedback moves a system closer to its set point, while negative feedback moves a system further from its set point. - Negative feedback requires the detection of stimuli, while positive feedback functions independently of stimuli. - Negative feedback reverses changes in a system, while positive feedback amplifies changes in a system. - Positive feedback occurs only in response to stimuli, while negative feedback can occur in the absence of stimuli.

Negative feedback reverses changes in a system, while positive feedback amplifies changes in a system.

During cell communication in the nervous system, chemical messengers called neurotransmitters travel between neurons. As they travel, neurotransmitters send messages from one neuron to another. Which of the following best describes the role of neurotransmitters in neuron-to-neuron communication? - Neurotransmitters are long-distance signaling molecules that allow neurons to communicate over long distances. - Neurotransmitters are local regulators that allow neurons to communicate over long distances. - Neurotransmitters are long-distance signaling molecules that allow neurons to communicate over short distances. - Neurotransmitters are local regulators that allow neurons to communicate over short distances.

Neurotransmitters are local regulators that allow neurons to communicate over short distances.

To complete external fertilization in fish, sperm cells must swim through open water in order to fertilize egg cells. During this process, females release a substance called ovarian fluid, which helps guide the sperm cells toward the egg cells. Researchers hypothesized that sperm cells are mainly attracted by ovarian fluid released from the same species. To test this hypothesis, researchers performed an experiment in which they studied the effects of salmon ovarian fluid and trout ovarian fluid on salmon sperm. In each trial within the experiment, the researchers placed salmon sperm on one side of a porous membrane and either salmon ovarian fluid, trout ovarian fluid, or water on the other side. After two minutes, the researchers counted how many salmon sperm had passed through the membrane and into the fluid. The results are presented in the graph below. Which of the following conclusions is best supported by the data above? - Salmon sperm respond more strongly to long-distance signaling molecules in trout ovarian fluid than to those in salmon ovarian fluid. - Salmon sperm respond more strongly to local regulators in trout ovarian fluid than to those in salmon ovarian fluid. - Salmon sperm respond more strongly to long-distance signaling molecules in salmon ovarian fluid than to those in trout ovarian fluid. - Salmon sperm respond more strongly to local regulators in salmon ovarian fluid than to those in trout ovarian fluid.

Salmon sperm respond more strongly to long-distance signaling molecules in salmon ovarian fluid than to those in trout ovarian fluid.

Mutations within genes coding for G protein-coupled receptors (GPCRs) can lead to one of two major outcomes—a loss-of-function or a gain-of-function. Loss-of-function mutations prevent signaling in GPCR pathways, even in the presence of signaling molecules. Gain-of-function mutations activate signaling in GPCR pathways, even in the absence of signaling molecules. Which of the following is most likely to result from a loss-of-function GPCR mutation? - Signal transduction pathways that are activated by multiple types of ligands - Signal transduction pathways that are inactive only if ligand-to-receptor binding does not occur - Signal transduction pathways that are inactive even if ligand-to-receptor binding occurs - Signal transduction pathways that are activated without ligand-to-receptor binding

Signal transduction pathways that are inactive even if ligand-to-receptor binding occurs

Many species of bacteria regulate gene expression using a cell signaling system known as quorum sensing (QS). In this system, bacteria synthesize QS signaling molecules and release them into the surrounding environment. The effects of these molecules on gene expression depend on the density of the bacterial population. Which of the following best describes what occurs as the density of a QS bacterial population increases? - The concentration of QS signaling molecules increases, eventually triggering a change in gene expression throughout the bacterial population. - The concentration of QS signaling molecules increases, eventually triggering a change in gene expression in a few members of the bacterial population. - The concentration of QS signaling molecules decreases, eventually triggering a change in gene expression throughout the bacterial population. - The concentration of QS signaling molecules decreases, eventually triggering a change in gene expression in a few members of the bacterial population.

The concentration of QS signaling molecules increases, eventually triggering a change in gene expression throughout the bacterial population.

During the humoral immune response, helper T-cells activate B-cells through cell communication. This process is shown in the image below. During an experiment, researchers introduced a substance that caused the T-cell receptor to break down. Which of the following best describes how the humoral immune response will be affected? - The helper-T cell still binds to the B-cell, but B-cell will instead be activated by the killer-T cell. - The helper-T cell will no longer bind the B-cell, but instead the helper-B cell will be activated by helper-T cell by releasing long-distance signals. - The helper-T cell will no longer bind to the B-cell, as a result, B-cell will not be activated. - The helper-T cell will bind to the B-cell, but B-cell will not be activated.

The helper-T cell will no longer bind to the B-cell, as a result, B-cell will not be activated.

During the cell-mediated immune response, killer T-cells target and kill infected cells. This process is shown in the image below. During an experiment, researchers introduced a substance that caused the Class I MHC molecule to break down. Which of the following best describes how the cell-mediated immune response will be affected? - The killer T-cell will still bind to the infected cell, but the infected cell will instead be killed by a helper T-cell. - The killer T-cell will no longer bind to the infected cell, and the infected cell will instead be killed by killer T-cells releasing long-distance signals. - The killer T-cell will still bind to the infected cell, but the infected cell will not be killed. - The killer T-cell will no longer bind to the infected cell, and as a result, the infected cell will not be killed.

The killer T-cell will no longer bind to the infected cell, and as a result, the infected cell will not be killed.

A mutation causes the extracellular domain of a G protein-coupled receptor (GPCR) to be misfolded. The misfolded GPCR is packaged into a vesicle that travels to the cell membrane. Upon reaching the cell membrane, the vesicle deposits the misfolded GPCR, which fuses with the cell membrane and functions as a membrane receptor. Which of the following best predicts what will occur whenever the misfolded GPCR is in the presence of its specific ligand? - The extracellular domain of the misfolded GPCR will begin a signal transduction pathway. - The intracellular domain of the misfolded GPCR will not bind with its specific ligand. - The intracellular domain of the misfolded GPCR will change from an inactive to an active shape. - The ligand-binding domain of the misfolded GPCR will not bind with its specific ligand.

The ligand-binding domain of the misfolded GPCR will not bind with its specific ligand.

The tobacco mosaic virus (TMV) is a plant virus that infects a wide range of plants, including tobacco. In order to enter and travel through the cells of a plant, TMV produces a movement protein. This protein helps the virus travel directly between the cytoplasms of interconnected plant cells. Which of the following best predicts how the movement protein modifies plant cells in order to help TMV travel from cell-to-cell? - The movement protein modifies the plasmodesmata between plant cells. - The movement protein increases the formation of transport vesicles within plant cells. - The movement protein modifies the vacuoles within plant cells. - The movement protein increases the formation of cell walls between plant cells.

The movement protein modifies the plasmodesmata between plant cells.

The diagram above represents a model of a signal transduction pathway in a cell that is targeted by two different ligands,L1 and L2. When L1 binds with membrane receptorR1start subscript, 1, end subscript, the pathway is activated, and CDK activity in the cell increases. Alternatively, when L2 binds with membrane receptor R2, downstream signaling by the pathway is inhibited. Based on the model above, what would most likely result if a mutation prevents the binding of L2 with R2? - The signal transduction pathway would be inhibited, resulting in increased cell division. - The signal transduction pathway would proceed unchecked, resulting in decreased cell division. - The signal transduction pathway would proceed unchecked, resulting in increased cell division. - The signal transduction pathway would be inhibited, resulting in decreased cell division.

The signal transduction pathway would proceed unchecked, resulting in increased cell division.

Researchers studying cell cycle regulation in budding yeast have observed that a mutation in the CDC15 gene causes cell cycle arrest in telophase when the yeast cells are incubated at an elevated temperature. Which of the following statements best predicts the effect of the cell cycle arrest on proliferating yeast cells? - The yeast cells will transition out of G0 but will fail to complete the G1 phase. - The yeast cells will initiate mitosis but will fail to complete the G2 phase. - The yeast cells will replicate their chromosomes but will fail to complete cytokinesis - The yeast cells will replicate their organelles but will fail to complete the S phase.

The yeast cells will replicate their chromosomes but will fail to complete cytokinesis

In response to stress, the hypothalamic-pituitary-adrenal (HPA) axis coordinates the release of the steroid hormone cortisol, as summarized in the figure above. Inhaled corticosteroids (ICS) are a class of synthetic steroid hormones that are commonly used in the long-term treatment of persistent asthma. Assuming that ICS function in the same way as naturally occurring cortisol, it is most likely that long-term, high-dose ICS use would - stimulate CRH production - reduce cortisol production - stimulate cortisol production - stimulate ACTH production

reduce cortisol production