3 questions, one for each idea where we can. Answer them, then see which ideas to fix.
Question 1 of 3
During the development of a human hand, cells in the tissue between the developing fingers receive chemical signals that cause them to undergo apoptosis, and the fingers become separate. Which statement best describes apoptosis?
Answer and reasoning
AA regulated process in which signals lead a cell to take itself apart in an orderly wayCorrect Apoptosis is programmed cell death: signals trigger a pathway in the cell that leads to its orderly, regulated self-destruction. Here it removes the tissue between the fingers as a normal part of development.
BAn uncontrolled death in which a cell that has been injured swells up and then bursts open A student who thinks apoptosis is the same as death from injury picks this. Swelling and bursting after injury is uncontrolled death; apoptosis is a regulated response to signals, and the cells between the fingers are not injured.
CA breakdown of normal cell signaling that occurs in diseased tissue and so harms the body A student who thinks cell death is always harmful picks this. The stem describes apoptosis in normal development: it is how the fingers become separate, not a sign of disease.
DA process in which the signal molecules enter the cell and digest it from the inside A student who thinks the signal molecule itself carries out the response picks this. The signals trigger a pathway, and the cell's own proteins carry out its orderly self-destruction; the signal molecules do not digest the cell.
In a hypothetical species of yeast, a peptide signal, P, binds to a receptor in the plasma membrane and triggers production of enzyme E. Mutant 1 has a mutation in the receptor's ligand-binding domain; mutant 2 has a mutation in the receptor's intracellular domain. The graph shows the activity of enzyme E in wild-type and mutant cells grown with different concentrations of P. Which statement is supported by the data?
Answer and reasoning
AMutant 2 makes a high level of enzyme E even when there is no P in the medium.Correct At 0 nM P, mutant 2's activity is about 86 units, compared with 5 in the wild type, and it stays high at every concentration. The mutation in the intracellular domain leaves the receptor relaying a signal without the ligand, so the pathway is active without P.
BBoth mutants make less enzyme E than the wild type when P is present. A student who thinks mutations can only reduce signaling picks this. Mutant 2 makes more enzyme E than the wild type at every concentration of P, with or without P present.
COnly mutant 1, whose mutation is in the binding domain, differs from wild type. A student who thinks only the ligand-binding domain affects signaling picks this. Mutant 2, whose mutation is in the intracellular domain, differs most from the wild type at low concentrations of P.
DWild-type activity rises by about the same amount for each 2 nM of P added. A student who expects a straight-line relationship picks this. Wild-type activity rises by 25 units from 0 to 2 nM but by only 2 units from 8 to 10 nM; the curve levels off.
Chemical K binds to a protein kinase in a signaling pathway inside a cell and prevents the kinase from being activated. K does not bind to the receptor. Which statement best explains how K can block the cell's response to the pathway's ligand?
Answer and reasoning
AK keeps the kinase from relaying the signal to the components after it, so they stay inactive.Correct In a signal transduction pathway, each component is activated by the one before it. With the kinase blocked, the components after it are not activated, so the signal does not reach the response, even though the ligand still binds the receptor.
BK stops the ligand molecule itself from moving down the pathway toward the nucleus of the cell. A student who thinks the ligand itself travels along the pathway picks this. The ligand binds the receptor; what passes along the pathway is a series of changes in the cell's proteins.
CK stops the receptor from binding its ligand, since the kinase controls the receptor. A student who thinks a block at a later step stops the earlier steps picks this. The kinase is activated after the receptor, so blocking it does not affect ligand binding.
DK unfolds the three-dimensional structure of the kinase and of every other protein in the pathway. A student who thinks inhibitors work by denaturing proteins picks this. K binds to the kinase and prevents its activation; it does not unfold the pathway's proteins.
In preparation: 0 of 3 sections compiled and reviewed. The rest show key terms and common mistakes from our question bank until they are.
4.3.A.1 Signal transduction pathway Fix
Signal transduction pathway
The series of steps by which a signal received at a receptor is relayed inside a target cell, often through protein modifications such as phosphorylation and second messengers such as cAMP, and often amplified, producing a cellular response.
Cellular response
The change in a target cell that a signal transduction pathway produces. It may be a change in gene expression (which proteins the cell makes, and how much), a change in cell function (such as enzyme activity, secretion, contraction or cell division), a change in phenotype, or apoptosis.
Gene expression
The use of the information in a gene to make a functional product, such as a protein. A signal can change which genes a cell expresses, and how much, without changing the DNA sequence of those genes.
Apoptosis
Programmed cell death: an orderly, regulated process, triggered through signaling pathways, in which a cell dismantles itself. It removes cells as a normal part of development, such as the tissue between developing fingers, and it removes damaged or unneeded cells.
Phenotype
The observable characteristics of a cell or organism. A signal that changes gene expression or cell function can change a cell's phenotype, for example by changing which enzymes it contains.
Quorum sensing
Cell-to-cell communication in which bacteria release a signal molecule whose concentration in the surroundings rises as the population grows. Above a threshold concentration, the signal triggers a response in the cells, such as a change in gene expression, so the population responds to its own density.
Error bars of ±2 SE
Bars extending two standard errors of the mean above and below a sample mean, an approximate 95% confidence interval. When the bars of two means do not overlap, the difference is likely to be real; when they overlap, the data do not establish a difference.
Students often think The signal molecule itself does the work of the response: it enters the cell or passes along the pathway and directly produces the effect, such as breaking down glycogen, giving off light or destroying the cell. In fact No. The ligand binds to a receptor, and the response is carried out by the cell's own proteins after the signal has been relayed. A ligand that binds a receptor in the plasma membrane does not need to enter the cell; what passes inward is a series of changes in the cell's proteins.
Students often think Different cell types contain different genes: each type of cell keeps only the genes it uses. In fact No. Nearly all the cells of a multicellular organism carry the same genes. Different cell types express different sets of these genes, so they contain different receptors, relay proteins and target proteins and can respond differently to the same signal.
4.3.B.1 Receptor domains Fix
Receptor domains
Regions of a receptor protein with different roles. The ligand-binding domain recognizes the ligand. In a receptor in the plasma membrane, a transmembrane domain spans the membrane and an intracellular domain changes shape when the ligand binds, starting transduction. A mutation in any domain may alter how the signal is transduced.
Relay protein
A protein in a signal transduction pathway, such as a protein kinase, that is activated by the component before it and activates the component after it, passing the signal along. If it cannot be activated, the components after it are not activated either.
Activating mutation
A mutation that leaves a receptor or another pathway component in its active form even when no ligand is bound, so the components after it, and the response, are active without the signal.
Students often think Only the ligand-binding domain matters for signaling: a mutation elsewhere in the receptor has no effect, and a mutation that changes signaling must have changed how the ligand binds. In fact No. The transmembrane and intracellular domains pass the signal on after the ligand binds, so a mutation in any domain may change how the signal is transduced, even when the ligand still binds.
Students often think Mutations in a signaling pathway can only reduce or block signaling; they cannot make the pathway more active. In fact Yes. Some mutations leave a receptor or relay protein in its active shape, so the pathway is active and the response occurs even without the ligand. Other mutations reduce or block signaling, and some have little effect.
4.3.B.2 Pathway inhibitor Fix
Pathway inhibitor
A chemical that interacts with a component of a signaling pathway, such as the receptor or a relay protein, and reduces the pathway's activity. Some compete with the ligand for its binding site; others act elsewhere on the receptor or at a later step.
Pathway activator
A chemical that interacts with a component of a signaling pathway and increases its activity. An activator that acts on a component after the receptor can produce the response without the ligand.
Solvent (vehicle) control
A control group that receives the solvent used to deliver a test chemical, without the chemical, and is otherwise treated like the experimental group, so that any effect of the solvent itself is not mistaken for an effect of the chemical.
Students often think A pathway's response can occur only when the ligand is bound to the receptor; a chemical that does not act like the ligand cannot activate the pathway. In fact No. A chemical or a mutation that activates a component after the receptor can produce the response without the ligand, because the later components respond to the component before them, not to the ligand.
Students often think Inhibitors work by denaturing proteins: a chemical that blocks a pathway unfolds the proteins of the pathway. In fact No. An inhibitor binds to a particular component, at a ligand-binding site, an allosteric site or a site on a relay protein, and reduces that component's activity while the protein keeps its overall folded structure. Denaturation is the loss of the folded structure itself.
9 more questions. Every wrong answer here is a real mistake students make, and you see why it is wrong as soon as you answer.
Question 1 of 9
Cultured cells from a hypothetical mammal were given one of four treatments: no addition (control); signal S, which binds to a receptor on the cell surface; signal S plus chemical X, which binds to the same receptor; or chemical X alone. After 24 hours, the percentage of cells undergoing apoptosis was measured. The graph shows the mean for each treatment (n = 5 cultures), with error bars representing ±2 SE of the mean. Which conclusion is best supported by the data?
Answer and reasoning
AX alone lowers apoptosis below the control level, as its mean is lower than the control's. A student who treats any difference between means as real picks this. The X bar (1.5–4.5) overlaps the control bar (2.5–5.5) widely, so the 1-point difference between the means could be due to chance variation.
BS plus X gives exactly the same apoptosis as the control, as their error bars overlap. A student who thinks overlapping error bars prove two means are equal picks this. Overlap shows only that a difference has not been established; the sample means (6 and 4) are not the same.
CS increases apoptosis, but not significantly with X present, as the S + X and control bars overlap.Correct The S bar (19–25) does not overlap the control bar (2.5–5.5), so S increases apoptosis. The S + X bar (4–8) overlaps the control bar, so when X occupies the receptor, S produces no significant increase: X prevents the response to S.
DS injures and damages the cells it binds to, as it raises apoptosis above the control level. A student who thinks apoptosis is death caused by injury picks this. Apoptosis is a regulated response that a signal can trigger in undamaged cells; the rise in apoptosis shows a response to S, not damage.
Working No test statistic is calculated; the decision rests on the ±2 SE error bars. Control 4 (2.5–5.5); S 22 (19–25); S + X 6 (4–8); X 3 (1.5–4.5). S vs control: the bars do not overlap (19 > 5.5), so S increases apoptosis. S + X vs control: the bars overlap (4–5.5), so with X present S produces no significant increase. X vs control: the bars overlap widely, so X alone has no shown effect; a 1-point lower mean is not evidence of a difference, and overlap does not show the means are exactly equal. Apoptosis is a regulated response to the signal, so the rise does not show injury.
The model shows how epinephrine, a hormone carried in the blood, acts on a liver cell and on a heart muscle cell. Based on the model, which statement best explains why epinephrine causes different responses in the two cell types?
Answer and reasoning
AEpinephrine itself breaks down glycogen in one cell and makes the other contract. A student who thinks the signal molecule itself carries out the response picks this. In the model, epinephrine binds to the receptor outside the cell; the responses are carried out by the cells' own proteins at the end of each pathway.
BThe protein kinase acts on different target proteins in the two types of cell.Correct In the model, both cells relay the signal through the same kinds of steps, from receptor to protein kinase, but the kinase acts on glycogen-breakdown enzymes in the liver cell and on ion channel proteins in the heart cell. Different target proteins give different responses to the same signal.
CThe two types of cell carry different genes, since each keeps only the genes it uses. A student who thinks different cell types contain different genes picks this. Liver and heart cells carry the same genes; they differ in which genes they express, so they contain different target proteins.
DEach type of cell chooses the response that will best meet the overall needs of the body. A student who explains cell responses by what the body needs picks this. A cell does not choose; its response follows from the proteins its pathway contains, as the model shows.
In a hypothetical species of marine bacterium, cells produce light only when the population is dense. A student claims that light production is a response to a signal molecule that the cells release into the medium and that builds up as the population grows. Low-density cultures were grown in different media, and a mutant strain that cannot make the signal molecule was used to prepare one medium. The table shows the results. Which reasoning best connects the evidence to the student's claim?
Answer and reasoning
AThe signal molecules themselves give off light, so light appears once enough of them build up in the medium around the cells. A student who thinks the signal molecule itself carries out the response picks this. Purified signal in medium without cells gave no light, so the light is produced by the cells in response to the signal.
BThe medium from dense cultures causes mutations in the sparse cells that permanently switch on the genes for light. A student who thinks a signal changes a cell's DNA picks this. A signal changes which genes a cell expresses, not the DNA sequence; the evidence shows a response to the signal, not a change in the cells' genes.
COnly the culture in medium from a dense culture is needed, as its bright light on its own proves the claim. A student who thinks a single treated group can show an effect picks this. Without the fresh-medium and mutant-medium results, the light could be caused by something else in the medium, such as nutrients; the comparisons are what link the light to the signal.
DSparse cells made light only with the signal present, so the signal acts through a pathway in each cell to switch on light.Correct Low-density cells made light with medium from a dense culture or with purified signal, but not with fresh medium or with medium from the mutant that cannot make the signal, and the signal alone, without cells, gave no light. The signal molecule, not crowding, triggers a response in the cells: it acts through a signaling pathway that changes what the cells do.
The model shows a signal transduction pathway in a hypothetical animal cell. Cells with a mutation in the intracellular domain of receptor R, and cells with a mutation that inactivates protein A, both fail to respond to ligand L. Based on the model, which statement best explains why the two mutations have the same effect?
Answer and reasoning
AAny mutation in a signaling pathway blocks it, wherever in the pathway it lies. A student who thinks mutations can only reduce or block signaling picks this. Some mutations leave a component in its active form and switch the pathway on; these two mutations have the same effect because, in the model, the intracellular domain and protein A are links in the same chain to protein B.
BL enters the cell and binds to A, so A acts as a second receptor for ligand L. A student who thinks the ligand itself travels into the cell picks this. In the model, L binds to the receptor's ligand-binding domain outside the cell; protein A is activated by the receptor's intracellular domain.
CA controls R, so a defect in A stops R from binding L at the cell's surface. A student who thinks a defect in a later component stops earlier steps picks this. In the model, the arrows run from R to A, not from A to R; R can still bind L when A is inactive.
DR's intracellular domain and A are each needed to pass the signal to B.Correct In the model, the signal passes from the intracellular domain of R to protein A and then to protein B. Both are links in the same chain, so a defect in either stops protein B and the response from being activated.
In a hypothetical animal cell, ligand L binds to receptor R, which activates protein A. Active A activates two proteins: protein B, which leads to glycogen breakdown, and protein C, which leads to changes in gene expression. A mutation inactivates protein C; receptor R, A and B are normal. Which prediction about the cell's response to L is best supported?
Answer and reasoning
ANeither response occurs, as inactive C blocks the pathway all the way back to R. A student who thinks a defect in a later component stops the earlier steps picks this. The signal passes from R to A and then to B and C; inactive C does not affect R, A or B.
BGlycogen breakdown still occurs, but the changes in gene expression do not occur.Correct Protein C lies on the branch that leads only to changes in gene expression. R, A and B are normal, so L still activates the branch through B and glycogen is broken down; without active C, the gene-expression response is lost.
CBoth responses occur normally, since the receptor and its binding domain are unchanged. A student who thinks only the receptor's binding domain affects signaling picks this. A mutation in any component of the pathway can alter the responses after it; here, C is needed for the changes in gene expression.
DGene expression changes fail, and glycogen breakdown rises to make up for the loss. A student who thinks cells make up for a failed pathway because they need to picks this. Nothing in the pathway increases the activation of B when C is inactive; glycogen breakdown occurs as normal.
The part of a hormone receptor that spans the plasma membrane contains amino acids with nonpolar R groups. A mutation replaces one of these with an amino acid that has a charged R group. Cells with the mutant receptor no longer respond to the hormone. Which explanation is best supported?
Answer and reasoning
AThe charged R group must change the shape of the hormone-binding site, as binding is the only step a mutation can affect. A student who thinks a receptor mutation can affect signaling only by changing ligand binding picks this. The charged R group is in the part that spans the membrane, not in the hormone-binding site, and a mutation in any domain of a receptor may alter transduction of the signal after the hormone binds.
BThe hormone is now unable to pass through the receptor and across the membrane to act on proteins in the cell. A student who thinks a ligand travels through its receptor into the cell picks this. A hormone that binds a receptor in the plasma membrane does not pass through it; the receptor changes shape and relays the signal.
CThe charged R group disrupts how the receptor sits in the membrane, so the signal is not passed to the inside of the cell.Correct The transmembrane domain lies in the nonpolar interior of the membrane, where a charged R group is unfavorable. Disrupting this domain changes how the receptor sits in the membrane, so the change in shape caused by hormone binding is not passed to the intracellular domain and the signal is not transduced.
DThe cells stopped responding to the hormone because they have stopped needing the signal it carries to them. A student who explains cell responses by what cells need picks this. The cells stop responding because the mutation alters the receptor, not because of any need.
A researcher tests whether chemical Z inhibits a signaling pathway that ligand L activates in a hypothetical cell line. Z does not dissolve in water, so it is dissolved in a solvent before it is added. The experimental group is cells given L plus Z dissolved in the solvent, and the response is measured after 1 hour. Which group is the most appropriate control?
Answer and reasoning
ACells given nothing at all: no L, no Z and no solvent added A student who thinks the control is the group to which nothing is added picks this. This group differs from the experimental group in three ways, lacking L, Z and the solvent, so a difference could not be attributed to Z.
BCells given L plus the same volume of solvent, with no ZCorrect This group differs from the experimental group only in lacking Z: it gets the same ligand, the same solvent and the same timing. A smaller response in the experimental group can then be attributed to Z rather than to the solvent.
CCells given L plus Z dissolved in the solvent, at half the dose A student who thinks the control should receive the treatment picks this. Cells given Z at a lower dose still receive Z, so they cannot show the response without it.
DCells given L plus Z in the solvent, measured at 0 hours and at 1 hour A student who thinks a treated group alone can show an effect picks this. Measuring the same treated cells twice gives no group without Z to compare with, so a small response could not be attributed to Z rather than to the solvent or to time.
Cells of a hypothetical cell line were exposed to chemical P or chemical Q at different concentrations. Cells given P received no ligand; cells given Q also received the pathway's ligand, L, at a fixed concentration. The graph shows the response of the cells as a percentage of the maximum response to L. Which statement is supported by the data?
Answer and reasoning
AP has no effect on the cells unless the ligand, L, is also present. A student who thinks a pathway's response must begin with the ligand binding its receptor picks this. P was given with no L at all, yet the response rose to 80%.
BP and Q both inhibit the pathway, so the response falls as they rise. A student who thinks chemicals that act on a pathway can only inhibit it picks this. The response rises as P rises; only Q lowers it.
CP produces a response without L, and Q reduces the response to L.Correct Without any ligand, the response rises from 0 to 80% as P rises from 0 to 40 μM, so P activates the pathway. With L present, the response falls from 100% to 10% as Q rises, so Q inhibits it. Chemicals that interact with a pathway can activate or inhibit it.
DEach chemical changes the response by the same amount per 10 μM. A student who expects straight-line relationships picks this. P raises the response by 10 points from 0 to 10 μM but by 30 points from 10 to 20 μM; the changes are not equal.
In a hypothetical cell line, ligand L binds to receptor R, R activates protein A, and A activates protein B, which causes the response. Chemical Z blocks the response to L. A student claims that Z acts at a step after the receptor, not on R itself. Which observation, if made, would best support the student's claim?
Answer and reasoning
ARaising the concentration of L, even greatly, does not overcome Z's effect on the response. A student who thinks extra ligand overcomes any inhibitor acting on the receptor picks this. An inhibitor bound to another site on R would not be overcome by more L either, so this does not show that Z acts after R.
BCells treated with both Z and L show little or no response to the ligand L. A student who thinks one treated group can show an effect picks this. This only repeats that Z blocks the response; it says nothing about where Z acts.
CWith Z present, ligand L can no longer bind to receptor R on the cell surface. A student who thinks a block at a later step stops ligand binding picks this. Loss of L binding would point to Z acting on R itself, the opposite of the claim.
DZ also blocks the response caused by a chemical that activates A directly, with no L.Correct A chemical that activates A directly produces the response without L or R. If Z still blocks this response, Z must act at A, at B or at a later step, after the receptor, which supports the claim.
Working No calculation. To show that Z acts after R, the response must be started without R: a chemical that activates A directly bypasses R, so if Z still blocks that response, Z acts at A, at B or later. Failure of extra L to overcome Z fits an inhibitor at an allosteric site on R as well as one acting later; a treated group alone gives no comparison and says nothing about where Z acts; and loss of L binding would point to action on R, the opposite of the claim.
Compiled from the AP Biology Course and Exam Description (effective Fall 2025) and our question bank · Specialist review in progress. How these pages are made · Free, no account
