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22 questions
Following surgical removal of the thyroid gland, the level of thyroid-stimulating hormone (TSH) in the blood will increase. Which of the following best explains this increase?
Residual blood thyroxine, from prior to thyroid gland removal, will bind to cells in the anterior pituitary, signaling more TSH secretion.
Thyroxine will remain bound to thyroxine receptors on various body cells, and these body cells will secrete additional hormones that stimulate the anterior pituitary to secrete TSH.
Thyroxine that was stored in the anterior pituitary prior to thyroid gland removal will signal more TSH secretion.
A decrease in thyroxine levels means a loss of inhibition to the hypothalamus and anterior pituitary, leading to increased TSH secretion.
In mammals, an increase in the concentration of sodium in the blood triggers the release of antidiuretic hormone (ADH) from the pituitary gland. As the concentration of sodium in the blood returns to previous levels, the release of ADH from the pituitary gland is reduced. Based on the information presented, which of the following describes the most likely role of ADH in maintaining blood osmolarity?
ADH promotes an increase in the movement of sodium into the bloodstream.
ADH promotes an increase in the movement of water into the bloodstream.
ADH promotes an increase in the excretion of water from the body.
ADH promotes an increase in the secretion of additional ADH from the pituitary gland.
Which of the following best describes how the amount of DNA in the cell changes during M phase?
The amount of DNA doubles as the DNA is replicated
The amount of DNA slightly increases as a result of new organelle synthesis.
The amount of DNA does not change while the cell grows.
The amount of DNA is halved as the cell divides into two daughter cells
As shown in the diagram above, when there is low fixed nitrogen in the environment, an increase in the concentration of free calcium ions and 2-oxyglutarate stimulates the expression of genes that produce two transcription factors (NtcA and HetR) that promote the expression of genes responsible for heterocyst development. HetR also causes production of a signal, PatS, that prevents adjacent cells from developing as heterocysts.
Based on your understanding of the ways in which signal transmission mediates cell function, which of the following predictions is most consistent with the information given above?
In an environment with low fixed nitrogen, treating the Anabaena cells with a calcium-binding compound should prevent heterocyst differentiation.
A strain that overexpresses the patS gene should develop many more heterocysts in a low fixed nitrogen environment.
In an environment with abundant fixed nitrogen, free calcium levels should be high in all cells so that no heterocysts develop.
In environments with abundant fixed nitrogen, loss of the hetR gene should induce heterocyst development.
Antidiuretic hormone (ADH) is important in maintaining homeostasis in mammals. ADH is released from the hypothalamus in response to high tissue osmolarity. In response to ADH, the collecting duct and distal tubule in the kidney become more permeable to water, which increases water reabsorption into the capillaries. The amount of hormone released is controlled by a negative feedback loop.
Based on the model presented, which of the following statements expresses the proper relationship between osmolarity, ADH release, and urine production?
As tissue osmolarity rises, more ADH is released, causing less water to be excreted as urine.
As tissue osmolarity rises, less ADH is released, causing less water to be excreted as urine.
As tissue osmolarity rises, more ADH is released, causing more water to be excreted as urine.
As tissue osmolarity rises, less ADH is released, causing more water to be excreted as urine.
The model shown in the figure represents the role of two hormones, calcitonin and parathyroid hormone (PTH), in maintaining normal blood calcium levels in humans. If a dietary change results in an increase in blood calcium concentration above normal levels, which of the following is the most likely effect on calcium homeostasis?
Calcitonin levels will decline, thus stimulating the release of PTH.
Calcitonin levels will rise, thus promoting the deposit of calcium into bones.
PTH levels will decline, thus stimulating the loss of calcium from bones.
PTH levels will increase, thus preventing the release of calcitonin.
Cancer can result from a variety of different mutational events. Which of the following is LEAST likely to result in the initiation of a cancerous tumor?
A receptor mutation results in activation of a cell-division pathway in the absence of the appropriate ligand.
A mutation results in the loss of the ability to produce a tumor-suppressor protein.
A defect in a cell-cycle checkpoint prevents a cell from entering the S phase
At the anaphase checkpoint, separation of chromatids occurs without all centromeres being attached to kinetochore microtubules from both poles.
Most cells that have become transformed into cancer cells have which of the following characteristics when compared to normal, healthy cells?
Shorter cell cycle
More carefully regulated rates of cell division
Lower rates of mitosis
Higher rates of protein translation
Identical DNA
Researchers investigating the regulation of neurotransmitter release from presynaptic neurons proposed a model (Figure 1) in which CDK5, a protein expressed in axon terminals, inhibits the movement of synaptic vesicles to the presynaptic membrane. To test their model, the researchers used a modified version of green fluorescent protein (GFP). In slightly alkaline conditions, GFP exhibits a bright green fluorescence. In acidic conditions, GFP exhibits no fluorescence. Using standard techniques, the gene encoding GFP is easily introduced into living cells. By engineering the expression of GFP in laboratory-cultured nerve cells, the researchers found that a bright green fluorescence was exhibited only when a presynaptic neuron was given a certain stimulus. Which of the following observations best supports the hypothesis that CDK5 negatively regulates neurotransmitter release?
Introduction of CDK5 protein into neurons results in the movement of synaptic vesicles to the plasma membrane in the absence of any stimulus.
Uptake of a gene encoding CDK5 by neurons results in the movement of synaptic vesicles to the plasma membrane in the absence of any stimulus.
Suppression of CDK5 expression in neurons inhibits the movement of synaptic vesicles to the plasma membrane in response to a specific stimulus.
Inhibition of CDK5 activity in neurons increases the movement of synaptic vesicles to the plasma membrane in response to a specific stimulus.
Researchers investigating the regulation of neurotransmitter release from presynaptic neurons proposed a model (Figure 1) in which CDK5, a protein expressed in axon terminals, inhibits the movement of synaptic vesicles to the presynaptic membrane. To test their model, the researchers used a modified version of green fluorescent protein (GFP). In slightly alkaline conditions, GFP exhibits a bright green fluorescence. In acidic conditions, GFP exhibits no fluorescence. Using standard techniques, the gene encoding GFP is easily introduced into living cells. By engineering the expression of GFP in laboratory-cultured nerve cells, the researchers found that a bright green fluorescence was exhibited only when a presynaptic neuron was given a certain stimulus. Previous experiments indicate that CDK5 is active only when attached to a protein called p35. Which of the following best predicts how p35 might play a role in regulating neuron function?
Elevated intracellular levels of p35 result in increased synaptic activity
Degradation of p35 results in increased synaptic activity
Reabsorption of p35 from the synaptic cleft results in increased synaptic activity
Attachment of p35 to synaptic vesicles results in increased synaptic activity
Researchers investigating the regulation of neurotransmitter release from presynaptic neurons proposed a model (Figure 1) in which CDK5, a protein expressed in axon terminals, inhibits the movement of synaptic vesicles to the presynaptic membrane. To test their model, the researchers used a modified version of green fluorescent protein (GFP). In slightly alkaline conditions, GFP exhibits a bright green fluorescence. In acidic conditions, GFP exhibits no fluorescence. Using standard techniques, the gene encoding GFP is easily introduced into living cells. By engineering the expression of GFP in laboratory-cultured nerve cells, the researchers found that a bright green fluorescence was exhibited only when a presynaptic neuron was given a certain stimulus. Based on the model, which of the following best explains how regulation of neurotransmitter release might increase the range of responses to a stimulus in the nervous system?
In the absence of any stimulus, neurons can still release neurotransmitters.
Different neurons in the same neural network can release different amounts of neurotransmitter.
In the depolarization phase of an action potential, postsynaptic neurons can adjust the amount of neurotransmitter bound to receptors on their surface.
In the recovery phase following a stimulus, enzymes can be mobilized to degrade molecules present in the synaptic vesicles.
Many human cells can be stimulated to divide by hormonelike growth factors that bind to receptor proteins (R) on the plasma membrane and trigger an internal signal-transduction cascade. In many cases, however, the process of contact inhibition prevents mitosis when cells are in direct contact with one another. Contact inhibition occurs when proteins called cell adhesion molecules (CAMs) interact, causing them to change shape so that the growth-factor signaling proteins that normally associate with CAMs are replaced by another protein, called M. Both pathways are depicted in the figures. Which of the following statements accurately uses the information presented to support the hypothesis that interruption of M function in a single body cell can result in cancer?
Protein 3 will be prevented from interacting with CAMs, causing the cell cycle to stop permanently.
The ras protein will remain bound to DNA, blocking expression of genes required for mitosis.
Growth-factor signaling can trigger mitosis in cells that are in direct contact with other cells.
The receptor proteins of body cells will no longer bind to growth-factor proteins.
Cell communication is critical for the function of both unicellular and multicellular eukaryotes. Which of the following is likely true of cell signaling?
Cell signaling uses the highest molecular weight molecules found in living cells.
Cell signaling has largely been replaced by other cell functions in higher mammals.
Similar cell signaling pathways in diverse eukaryotes are evidence of conserved evolutionary processes.
Cell signaling functions mainly during early developmental stages.
Researchers performed an experiment to determine the effect of certain genetic mutations on mitosis in tropical fruit fly embryos. They determined the percentage of cells in each of four phases of mitosis as shown in Figure 1. Which of the following patterns is shown by the data?
Mutant 1 cells are more similar to mutant 3 cells than to wild-type cells.
In wild-type cells, the percent of cells in anaphase is twice the amount of those in telophase
In mutant 3 cells, more time is spent in prophase/prometaphase than in the later stages of mitosis.
The percent of mutant 2 cells in anaphase is higher than that of mutant 1 cells.
What is the expected percent change in the DNA content of a typical eukaryotic cell as it progresses through the cell cycle from the start of the G1 phase to the end of the G2 phase?
−100%
−50%
+50%
+100%
If chemical signals in the cytoplasm control the progression of a cell to the M phase of the cell cycle, then fusion of a cell in G1 with a cell in early M phase would most likely result in the
replication of chromosomes only in the G1 cell
exiting of both cells from the cell cycle and into the G0 phase
condensation of chromatin in preparation of nuclear division in both cells
transfer of organelles from the G1 cell to the cell in the M phase
Figure 1 shows the number of chromosomes observed in an actively dividing human cell at each stage of cell division. Which of the following presents a correct interpretation of the changes in chromosome number depicted in Figure 1 ?
DNA replication occurs between metaphase and anaphase, doubling the number of chromosomes. Between telophase and cytokinesis, the cell divides in two, with each cell receiving half of the replicated chromosomes.
New chromosomes formed during prophase are doubled during anaphase and are recombined before cytokinesis.
Chromosomes enter metaphase containing two chromatids attached by a centromere. During anaphase, the chromatids are separated, each becoming a chromosome. Cytokinesis distributes the chromosomes into two separate cells.
At anaphase a cell contains two identical copies of each chromosome, but following telophase, one of the copies is broken down into nucleotides.
Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B
B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A
A and sometimes stimulate increased growth of blood vessels into the tumors. Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant
Brec can trigger intracellular signaling in the absence of B. Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Based on the signaling model shown in Figure 1, describe the role of molecule B.
Molecule B is a cyclin and inhibits the receptor
Molecule B is a ligand and binds to the receptor and activates the receptor.
Molecule B is a cyclin and binds to the receptor and activates the receptor.
Molecule B is a ligand that inhibits the receptor
Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B
B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A
A and sometimes stimulate increased growth of blood vessels into the tumors. Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant
Brec can trigger intracellular signaling in the absence of B. Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Explain how the addition of a phosphate group to certain amino acids of Brec likely affects the tertiary structure and function of Brec.
Phosphate could change the structure of Brec and that affects how it interacts with other signaling molecules in the cell
Phosphate could change the charge of Brec and that affects how it interacts with other signaling molecules in the cell
All of the above
Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B
B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A
A and sometimes stimulate increased growth of blood vessels into the tumors. Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant
Brec can trigger intracellular signaling in the absence of B. Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Explain how the addition of a small RNA
RNA could prevent the activation of kinase D
D.
The small RNA could inhibit translation of a mRNA encoding one of the proteins in the pathway leading to kinase D activation
The small RNA could lead to degradation of a mRNA encoding a protein in the pathway leading to kinase D activation
All of the above
Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B
B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A
A and sometimes stimulate increased growth of blood vessels into the tumors. Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant
Brec can trigger intracellular signaling in the absence of B. Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Based on the proposed signaling pathway, predict the relative amount of phosphorylated to unphosphorylated kinase D in the Brec-WT cells when the cells are grown in nutrient broth lacking B.
There will be more unphosphorylated than phosphorylated kinase D
There will be more phosphorylated than unphosphorylated kinase D
Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B
B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A
A and sometimes stimulate increased growth of blood vessels into the tumors. Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant
Brec can trigger intracellular signaling in the absence of B. Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Cells are treated with a compound that prevents the inactivation of kinase D. Researchers claim that Brec-WT cells treated with this compound will stimulate blood vessel-forming cell division to the same degree as Brec-MUT cells do in the absence of B. Based on the information provided, provide reasoning to support their claim.
The researchers are wrong only the Brec-WT can have active kinase D, which leads to the expression of A, and the expression of A stimulates the blood vessel-forming cell division
The researchers are wrong only Brec-MUT have active kinase D, which leads to the expression of A, and the expression of A stimulates the blood vessel-forming cell division by both cell types.
Both cell types have active kinase D, which leads to the expression of A, and the expression of A stimulates the blood vessel-forming cell division by both cell types.
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