Unit 4: Cell Communication and Cell Cycle

Unit 4 covers how cells communicate through signal transduction pathways and how the cell cycle is regulated from interphase through mitosis. CED topics 4.1 through 4.6.

4.1 Cell Communication

Cells have two basic ways to reach each other. They can touch, or they can send a chemical message across a distance. Cell-to-cell contact is direct communication through touching. Chemical signaling means a released signal travels to target cells somewhere else.

Chemical signals sort by distance. Local regulators act on cells near the emitting cell. Neurotransmitters are the example you know best. The CED also lists plant immune responses, quorum sensing in bacteria, and morphogens in embryos as short-distance examples. Hormones travel long distances in the bloodstream. The CED examples are insulin, human growth hormone, thyroid hormones, testosterone, and estrogen.

One kind of contact signaling is worth knowing by name. Immune cells interact through cell-to-cell contact, including antigen-presenting cells, helper T cells, and killer T cells. The CED lists this as an illustrative example, which means you should recognize it but will not be asked for details beyond what is here.

4.2 Introduction to Signal Transduction

A signal transduction pathway links the reception of a signal to a cellular response. It runs in three stages, always in this order. Reception is when a target cell detects the signal. Transduction is when the signal is relayed and amplified inside the cell. Response is what the cell does at the end.

Reception starts with two players. The ligand is the chemical messenger, a peptide or small molecule. The receptor protein recognizes it through a ligand-binding domain. Receptors sit on the cell surface or inside the cell, in the cytoplasm or nucleus. A ligand that cannot cross the plasma membrane binds a surface receptor. A ligand that can cross the membrane may bind a receptor inside the cell instead.

Specificity comes from the match between the two. Only cells carrying the right receptor respond to a given ligand. That is why a hormone traveling everywhere in the blood still affects only its target cells. The signal is public. The ability to hear it is not.

4.3 Signal Transduction

Two receptor types do most of the work you need to know. A G protein-coupled receptor sits in the membrane of the target cell. When the ligand binds on the outside, the intracellular domain changes shape and starts transduction. A ligand-gated channel is also in the membrane, but binding opens or closes the channel itself.

Inside the cell, a signaling cascade relays the signal from the receptor to its target in a sequence of steps. Two tools carry it. Second messengers are small intracellular molecules, such as cyclic AMP (cAMP), that spread the signal inside the cell. A phosphorylation cascade adds phosphate groups to a series of proteins, and each activated protein can activate many copies of the next one. That multiplication is where most of the amplification happens.

The cellular response to signaling is whatever the cell does at the end of the pathway. Signal transduction can change gene expression and cell function, alter the phenotype, or trigger apoptosis, which is programmed cell death. The CED example is epinephrine stimulating glycogen breakdown in mammals. One hormone outside the cell leads to many glucose molecules released inside, which shows amplification in action.

4.4 Changes in Signal Transduction Pathways

Pathways can change, and the response changes with them. A mutation in any domain of a receptor protein, or in any component of a signaling pathway, can alter signal transduction downstream. Chemicals that interact with any component of the pathway can activate it or inhibit it.

Work through the logic in both directions. If a mutation prevents the ligand from binding, the pathway stays silent and the response never happens. If a mutation locks a component in its active shape, the pathway can fire without any signal at all. Exam questions often give you one of these two cases and ask for the outcome, so check which part of the pathway the change hits before you answer.

4.5 Feedback

Feedback is how biological systems regulate themselves. In negative feedback, the response reduces the initial stimulus. When a variable moves off its set point, the system pushes it back. In positive feedback, the response amplifies the stimulus. The variable moves further from the set point as the stimulus intensifies, and the system changes instead of stabilizing.

Homeostasis is the maintenance of stable internal conditions in response to internal and external change, and feedback is the mechanism that achieves it. It operates at the molecular, cellular, and organismal levels. The CED example is blood sugar regulation. When blood glucose rises, insulin is released and cells take up glucose, bringing the level back down. Glucagon acts in the other direction when glucose falls. The stimulus is reduced either way, which is what makes it negative feedback.

4.6 Cell Cycle Regulation

The cell cycle is the regulated series of events by which eukaryotic cells grow and reproduce. It alternates between interphase, when the cell grows and copies its DNA, and mitosis, when the copied genome is divided between two daughter cells.

Interphase has three stages, always in this order. In G1 phase the cell is metabolically active, duplicating organelles and cytosolic components. In S phase DNA replicates, and each chromosome becomes two sister chromatids joined at the centromere. In G2 phase the cell synthesizes proteins, produces ATP in large quantities, and replicates its centrosomes. Some cells leave the cycle for G0 phase, a stage where they no longer divide but can reenter the cell cycle if the right cues arrive.

Mitosis moves a complete genome into two genetically identical daughter cells. It also drives growth, tissue repair, and asexual reproduction. The stages are defined by what you would see under a microscope.

After the nucleus divides, cytokinesis divides the cytoplasm. In animal cells a cleavage furrow pinches the cell inward. In plant cells a cell plate forms across the middle. Either way the result is two new daughter cells.

Cell cycle checkpoints are the internal controls that regulate progress through the cycle. They are operated by two partners. Cyclins are proteins whose levels rise and fall through the cycle. Cyclin-dependent kinases (CDKs) are enzymes that, together with cyclins, drive events forward. Learn the partnership, not a list. The CED states that knowledge of specific cyclin-CDK pairs is beyond AP scope.

When these controls fail, division can run unchecked. Cancer is uncontrolled cell division resulting from disruptions to the cell cycle. A broken checkpoint lets a damaged cell keep dividing instead of pausing for repair or undergoing apoptosis.

Confusions That Cost Points

Most missed questions in this unit come from a short list of pairs that look alike under time pressure. Review each pair carefully so you can tell them apart when you see them in a question.

Practice Questions

Original questions written for this guide in the style of the AP exam. Answers and explanations are on the next page, so complete the questions before checking them.

Answer Key

1. B. Insulin travels in the bloodstream to distant targets, which makes it a hormone. The neurotransmitter acts only on a nearby cell, which makes it a local regulator. A conflates chemical with local. Distance is the sorting rule, not chemistry. C describes direct contact, which neither signal uses. D misapplies the hormone label. Neurons release many signal types, and this one acts locally.

2. B. A ligand that cannot cross the membrane must bind on the outside, at a cell-surface receptor. A reverses the rule. Intracellular receptors are for ligands that can cross the membrane. C skips reception entirely, which breaks the pathway order. D confuses the eventual response with the binding site. Gene expression changes happen downstream, after transduction.

3. A. Each step activating many copies of the next is how the pathway amplifies a small input into a large response. B is the trap. Phosphorylation is a reversible modification, and nothing here makes the response permanent. C is wrong because the cascade sits downstream of reception. The receptor is still required. D invents a transport job for kinases. The ligand stays outside the cell.

4. B. If the ligand cannot bind, the receptor never initiates transduction and the response never happens. A describes a different mutation, one that locks a component in its active shape and causes constant firing. That is the direction trap for this topic. C invents a compensatory mechanism the pathway does not include. D targets the wrong component. The defect is at reception, not in the second messengers.

5. B. The response reduces the initial stimulus. Rising glucose triggers a response that lowers glucose back toward the set point, which is negative feedback. A reverses the direction. Positive feedback would push glucose even higher. C mislabels insulin, which is a hormone, not a kinase, and names the wrong mechanism. D borrows a bacterial term for a mammalian process.

6. B. DNA replication happens in S phase, producing two sister chromatids joined at the centromere. A is the trap for students who remember G1 involves duplication. G1 duplicates organelles and cytosolic components, not DNA. C comes after replication. G2 handles protein synthesis and centrosome replication. D is mitosis, when chromatids separate. Replication is already finished by then.

7. C. Sister chromatids separating toward opposite poles defines anaphase. A is condensation and spindle formation. B is alignment at the equator. D is the trap. Telophase reforms the nuclear envelope, which happens after separation is complete.

8. A. Checkpoints are the internal controls that pause the cycle, and a damaged cell that divides anyway points to checkpoint failure. B divides the cytoplasm during cytokinesis. It does not inspect DNA. C belongs to signal transduction, a different process entirely. D organizes the spindle. It carries out separation but makes no go or no-go decisions.

One-Page Recall Check

Say each answer out loud before you look back, and mark the ones you cannot finish. Anything you cannot say out loud yet belongs in your flashcard deck. In Rycal, add those items to the Cell Communication and Cell Cycle deck and let spaced review bring them back over the next few days.

• Sort these by signaling distance, shortest to longest: cell-to-cell contact, local regulator, hormone. State what sets each apart.
• Explain why only some cells respond to a hormone that travels everywhere in the blood.
• Define ligand and receptor, then explain which one determines the specificity of the response.
• Walk through reception, transduction, and response using epinephrine and glycogen breakdown.
• Explain how a phosphorylation cascade amplifies a signal, and name one second messenger.
• Distinguish a G protein-coupled receptor from a ligand-gated channel by what happens right after the ligand binds.
• Explain how a mutation in a pathway component can silence a response in one case and activate it without a signal in another.
• Contrast negative and positive feedback by what happens to the initial stimulus in each.
• Explain homeostasis and the role of feedback in maintaining it.
• List G1, S, and G2 in order and state what the cell accomplishes in each.
• Explain what G0 is and how a cell in G0 differs from one in G1.
• For prophase, metaphase, anaphase, and telophase, state the one visible event that defines each stage.
• Distinguish mitosis from cytokinesis, and state how cytokinesis differs in plant and animal cells.
• Explain the jobs of cyclin and cyclin-dependent kinases, and why their interaction matters more than either protein alone.
• Explain how a disruption to cell cycle checkpoints can lead to cancer.

Key terms for this unit

Cell-to-cell contact, chemical signaling, local regulators, immune cell interaction, long-distance hormones, local signaling examples, signal transduction pathway, ligand, receptor protein, G protein-coupled receptor, signaling cascade, second messenger, phosphorylation cascade, ligand-gated channel, hormone, cellular response to signaling, signaling pathway disruption, quorum sensing, epinephrine and glycogen breakdown, negative feedback, positive feedback, homeostasis, blood sugar regulation, cell cycle, interphase, G1 phase, S phase, G2 phase, G0 phase, mitosis, prophase, metaphase, anaphase, telophase, cytokinesis, sister chromatid, centromere, mitotic spindle, centrosome, cell cycle checkpoint, cyclin, cyclin-dependent kinase, cancer, apoptosis.

About this guide. Written for Rycal and aligned to the College Board AP Biology course framework, Unit 4, topics 4.1-4.6. All questions and explanations are original Rycal writing. Rycal is independent and is not affiliated with or endorsed by the College Board.