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Quiz: Cell Signaling and Feedback

Test your understanding of signal transduction, receptor types, second messengers, feedback loops, and apoptosis with these review questions.

1. Which type of cell signaling involves a hormone released into the bloodstream to act on distant target cells?

  1. Paracrine signaling
  2. Autocrine signaling
  3. Synaptic signaling
  4. Endocrine signaling
Show Answer

The correct answer is D. Endocrine signaling releases hormones into the bloodstream, allowing them to travel throughout the body and act on distant target cells that express the appropriate receptor, as insulin does when it travels from the pancreas to muscle and liver cells. Paracrine and synaptic signaling act over short distances, while autocrine signaling involves a cell responding to its own secreted signal.

Concept Tested: Modes of cell communication (endocrine signaling)

2. What is the general term for the family of cysteine proteases that execute the ordered dismantling of a cell during apoptosis?

  1. Kinases
  2. Caspases
  3. Phosphatases
  4. G proteins
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The correct answer is B. Caspases are cysteine proteases that exist as inactive procaspases until activated in a self-amplifying cascade. Effector caspases cleave cytoskeletal proteins, activate CAD to fragment DNA, and flip phosphatidylserine to the outer membrane leaflet, marking the cell for clean phagocytic removal without triggering inflammation.

Concept Tested: Apoptosis and the caspase cascade

3. Why do hydrophobic signaling molecules such as steroid hormones rely on intracellular receptors rather than cell-surface receptors?

  1. They are hydrophobic and can diffuse directly across the lipid bilayer, so no membrane-bound receptor is required
  2. They are too large to bind any cell-surface receptor
  3. They require a G protein to be activated inside the cell
  4. They can only signal through second messengers like cAMP
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The correct answer is A. Because steroid and thyroid hormones are lipid-soluble, they can pass directly through the phospholipid bilayer without needing a surface receptor to transport or transduce their signal. Once inside the cell, they bind intracellular receptors that act directly as transcription factors in the nucleus, producing slower but longer-lasting changes in gene expression.

Concept Tested: Intracellular receptors

4. How does signal amplification occur during a GPCR-cAMP-PKA signaling cascade?

  1. Each ligand molecule binds exactly one receptor and produces exactly one response molecule
  2. The receptor itself directly enters the nucleus to alter gene expression, bypassing amplification
  3. Each activated molecule in the cascade activates multiple downstream molecules, so a single hormone-receptor binding event can generate thousands of second messenger molecules and activate many effector proteins
  4. Amplification occurs only during apoptosis, not during normal receptor signaling
Show Answer

The correct answer is C. A single hormone molecule activates one receptor, but that receptor can activate hundreds of G proteins, each of which activates adenylyl cyclase to produce many cAMP molecules over its active lifetime, and each activated PKA molecule phosphorylates multiple target proteins. This cascading, one-to-many relationship at each step is what allows a tiny extracellular signal to produce a large intracellular response.

Concept Tested: Second messengers and signal amplification

5. How do negative and positive feedback loops differ in their effect on the original stimulus?

  1. Negative feedback amplifies the stimulus; positive feedback opposes it
  2. Both negative and positive feedback amplify the stimulus equally
  3. Negative feedback only operates during development; positive feedback only operates in homeostasis
  4. Negative feedback opposes and reduces the original stimulus to maintain a set point, while positive feedback amplifies the stimulus, driving the system further from baseline
Show Answer

The correct answer is D. Negative feedback loops, such as blood glucose regulation and thermoregulation, reduce the original stimulus and return the system toward a stable set point, underlying homeostasis. Positive feedback loops, such as action potentials and childbirth, instead reinforce and amplify the stimulus, driving the system toward a new state in an all-or-nothing manner.

Concept Tested: Negative vs. positive feedback loops

6. A researcher treats cells with a drug that inhibits phosphodiesterase. What effect would this most likely have on cAMP signaling?

  1. cAMP levels would remain elevated longer, prolonging PKA activation and extending the cellular response
  2. cAMP would be degraded more quickly, shortening the cellular response
  3. The GPCR would become permanently unable to bind its ligand
  4. Adenylyl cyclase activity would be directly inhibited
Show Answer

The correct answer is A. Phosphodiesterase normally degrades cAMP, terminating the second messenger signal. Blocking this enzyme allows cAMP to persist longer after a GPCR is activated, which keeps PKA in its active state for an extended period and prolongs the downstream cellular response, a mechanism exploited by some drugs used in asthma and heart failure treatment.

Concept Tested: cAMP signaling and protein kinase A

7. A cancer cell carries a Ras mutation that prevents GTP hydrolysis, locking Ras in its active, GTP-bound state. What is the most likely effect on cell proliferation signaling?

  1. The cell would stop dividing because Ras could no longer be activated
  2. The MAPK cascade would only activate when growth factor is present, exactly as in normal cells
  3. Ras would remain permanently active, continuously driving the MAPK cascade and promoting uncontrolled cell proliferation regardless of growth factor presence
  4. The RTK receptor would be degraded and signaling would stop entirely
Show Answer

The correct answer is C. Normal Ras signaling is transient because Ras hydrolyzes its own bound GTP to GDP, switching itself off. A mutation that prevents this hydrolysis locks Ras in the active state, so the MAPK proliferation cascade runs continuously even without growth factor stimulation, a mechanism found in a substantial fraction of human cancers.

Concept Tested: Receptor tyrosine kinases and the Ras/MAPK pathway

8. A drug binds to and blocks the Fas death receptor on a cell's surface. What is the most likely effect when that cell is exposed to FasL (Fas ligand)?

  1. The intrinsic mitochondrial pathway would be activated instead to compensate
  2. DISC formation and caspase-8 activation would be blocked, preventing the extrinsic apoptosis pathway from proceeding
  3. Caspase-9 would be directly activated in place of caspase-8
  4. The cell would undergo necrosis instead of apoptosis
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The correct answer is B. The extrinsic apoptosis pathway depends on FasL binding the Fas death receptor to trigger formation of the death-inducing signaling complex (DISC), which activates initiator caspase-8. Blocking the Fas receptor prevents this binding step entirely, so DISC cannot form, caspase-8 is not activated, and the extrinsic apoptotic pathway cannot proceed through this route.

Concept Tested: Extrinsic apoptosis pathway

9. What is the key mechanistic distinction between GPCR signaling and RTK signaling?

  1. GPCRs are enzymes themselves that phosphorylate tyrosine residues, while RTKs require a separate G protein
  2. Both receptor types use an identical G protein-second messenger mechanism
  3. RTKs only function in the nucleus, while GPCRs function exclusively at the plasma membrane
  4. GPCRs require a separate G protein and typically signal through second messengers like cAMP, while RTKs are themselves enzymes that dimerize and autophosphorylate to create docking sites for downstream signaling proteins
Show Answer

The correct answer is D. GPCRs couple to a distinct trimeric G protein that, once activated, triggers production of second messengers such as cAMP. RTKs, in contrast, are themselves catalytically active kinases: ligand binding causes two receptor monomers to dimerize and phosphorylate each other's tyrosine residues, creating docking sites that recruit intracellular proteins directly, most notably activating the Ras/MAPK cascade.

Concept Tested: GPCR vs. RTK signaling mechanisms

10. Cancer cells that overexpress the anti-apoptotic protein Bcl-2 are often resistant to chemotherapy drugs that work by inducing apoptosis through the intrinsic pathway. Why?

  1. Bcl-2 blocks cytochrome c release from mitochondria, preventing apoptosome formation and caspase-9 activation, so intrinsic pathway apoptosis fails even when DNA damage signals are present
  2. Bcl-2 directly degrades p53, preventing any DNA damage response
  3. Bcl-2 activates caspase-8 prematurely, causing uncontrolled apoptosis
  4. Bcl-2 enhances phosphatidylserine flipping, accelerating macrophage phagocytosis of the cancer cell
Show Answer

The correct answer is A. The intrinsic apoptosis pathway depends on the release of cytochrome c from mitochondria to trigger apoptosome formation and activation of caspase-9. Anti-apoptotic Bcl-2 proteins block this cytochrome c release, so even when chemotherapy causes DNA damage that would normally push a cell toward apoptosis via p53 and pro-apoptotic Bax/Bak signaling, an overabundance of Bcl-2 prevents the mitochondrial trigger from ever firing.

Concept Tested: Intrinsic apoptosis pathway and Bcl-2 regulation