AP Biology - Unit 4 Study Guide
AP Biology • Unit 4

Cell Communication & Cell Cycle

Exam Weight: 10–15% • Topics 4.1 – 4.6
4.1

Cell Communication

Cells must communicate with each other to coordinate activities in multicellular organisms. This communication occurs through chemical signals that are detected by receptors.

Why Cells Communicate
  • Coordinate growth and development
  • Respond to environmental changes
  • Regulate metabolism and gene expression
  • Control immune responses
  • Enable reproduction and cell division
Types of Cell Signaling (By Distance)
Direct Contact
Cell-to-cell contact: Gap junctions (animals) or plasmodesmata (plants) allow direct cytoplasmic connection.

Cell surface markers: Membrane proteins on one cell bind to receptors on adjacent cells.

Local Signaling
Paracrine: Signal molecules diffuse to nearby cells (e.g., growth factors).

Autocrine: Cell signals itself — binds to its own receptors.

Synaptic: Neurotransmitters cross synaptic cleft to target cell.

Long-Distance Signaling
Endocrine (Hormonal): Hormones travel through bloodstream to distant target cells.

Examples: Insulin, adrenaline, estrogen

Quorum Sensing
Bacteria-specific: Bacteria release signaling molecules to "sense" population density and coordinate group behaviors.

Example: Biofilm formation

DIRECT CONTACT Gap junctions/ Plasmodesmata PARACRINE Signaling Target Local diffusion to nearby cells SYNAPTIC Neuron Target Neurotransmitters across synapse ENDOCRINE Gland Target Hormones through bloodstream Adjacent Local Long Distance
Cell signaling ranges from direct contact between adjacent cells to long-distance hormonal signaling through the bloodstream.
AP Exam Tip: Be able to identify the type of signaling based on context clues. "Nearby cells" = paracrine. "Through blood" = endocrine. "Across synapse" = synaptic. "Cell junction" = direct contact.
4.2

Introduction to Signal Transduction

Signal transduction is the process by which a cell converts an extracellular signal into a cellular response. This involves three main stages.

The Three Stages of Cell Signaling
1. RECEPTION
Signal molecule binds receptor
→
2. TRANSDUCTION
Signal relay via cascade
→
3. RESPONSE
Cell changes behavior
Types of Receptors
Receptor Type Location Ligand Type Example
G Protein-Coupled Receptor (GPCR) Plasma membrane Hydrophilic (can't enter cell) Adrenaline, many hormones
Receptor Tyrosine Kinase (RTK) Plasma membrane Hydrophilic Growth factors, insulin
Ligand-Gated Ion Channel Plasma membrane Hydrophilic (neurotransmitters) Acetylcholine receptor
Intracellular Receptor Cytoplasm or nucleus Hydrophobic (crosses membrane) Steroid hormones, thyroid hormone
PLASMA MEMBRANE EXTRACELLULAR INTRACELLULAR (Cytoplasm) GPCR G protein L RTK Kinase ION CHANNEL + + INTRACELLULAR To nucleus Activates G protein Cross-phosphorylation Ions flow through
GPCR RTK Ion Channel Intracellular Receptor
Key Vocabulary
Term Definition
Ligand The signaling molecule that binds to a receptor (hormone, neurotransmitter, etc.)
Receptor Protein that specifically binds to a ligand, triggering a response
Second Messenger Small molecules that relay signals inside the cell (e.g., cAMP, Ca²⁺, IP₃)
Kinase Enzyme that adds phosphate groups to proteins (phosphorylation)
Phosphatase Enzyme that removes phosphate groups (turns off signal)
Hydrophobic vs. Hydrophilic Signals:
• Hydrophobic (steroids): Can cross membrane → bind intracellular receptors → directly affect gene expression
• Hydrophilic (most hormones): Can't cross membrane → bind surface receptors → need signal transduction cascade
4.3

Signal Transduction Pathways

Signal transduction pathways amplify and relay signals through a series of molecular interactions, often involving phosphorylation cascades and second messengers.

Signal Amplification

A single signal molecule can trigger a massive cellular response because each step in the pathway activates multiple molecules at the next step.

1 signal → 10 enzymes → 100 enzymes → 1000s of products!
Phosphorylation Cascade

Many signal transduction pathways use a series of protein kinases that activate each other by adding phosphate groups.

1
Receptor activated → activates first kinase
2
Kinase 1 phosphorylates (activates) Kinase 2
3
Kinase 2 phosphorylates (activates) Kinase 3
4
Kinase 3 phosphorylates target proteins → CELLULAR RESPONSE

Note: Phosphatases can remove phosphate groups to turn OFF the pathway.

Common Second Messengers
cAMP

Cyclic AMP

Made by adenylyl cyclase; activates protein kinase A (PKA)

Ca²⁺

Calcium ions

Released from ER; activates many enzymes including calmodulin

IP₃ / DAG

From PIP₂

IP₃ releases Ca²⁺; DAG activates protein kinase C

The cAMP Pathway (G Protein Signaling) ① Ligand binds H GPCR ② G protein activates G protein (GDP→GTP) ③ Adenylyl cyclase AC ATP → cAMP ④ cAMP activates PKA cAMP PKA ⑤ Phosphorylates target proteins → CELLULAR RESPONSE AMPLIFICATION 1 hormone molecule ↓ Many cAMP molecules ↓ Millions of products!
The cAMP pathway demonstrates how a single hormone can trigger a massive cellular response through signal amplification at each step.
Examples of Cellular Responses
• Gene expression changes (transcription factors activated)
• Enzyme activation/deactivation
• Ion channel opening/closing
• Cytoskeleton rearrangement
• Cell division or apoptosis
Turning OFF the Signal
• GTPase: G protein hydrolyzes GTP → GDP (inactivates itself)
• Phosphodiesterase: Breaks down cAMP
• Phosphatases: Remove phosphate groups from proteins
• Receptor internalization: Receptor removed from membrane
AP Exam Tip: Know that signal transduction allows for specificity (only cells with the right receptor respond), amplification (small signal → big response), and regulation (can be turned on/off at multiple points).
4.4

Feedback

Organisms use feedback mechanisms to maintain homeostasis and regulate biological processes. There are two main types: negative feedback and positive feedback.

Negative Feedback
The output inhibits the process, bringing the system back to a set point. This maintains homeostasis.

Think: "Thermostat"

Too hot → AC turns on → cools down → AC turns off

Positive Feedback
The output amplifies the process, pushing the system further from the starting point. This drives processes to completion.

Think: "Avalanche"

Process starts → output increases process → even more output

NEGATIVE FEEDBACK STIMULUS Response Output ⊣ Inhibits Maintains homeostasis POSITIVE FEEDBACK STIMULUS Response MORE Output + Amplifies Drives to completion
Examples of Feedback in Biology
Type Example How It Works
Negative Feedback Blood glucose regulation High glucose → insulin released → glucose uptake → glucose drops → insulin stops
Body temperature Too hot → sweating → cools body → sweating stops
Thyroid hormone High T3/T4 → inhibits TSH release → less thyroid hormone produced
Positive Feedback Childbirth (oxytocin) Contractions → oxytocin release → stronger contractions → more oxytocin
Blood clotting Injury → clotting factors → more clotting factors recruited → clot forms
Fruit ripening Ethylene → ripening → more ethylene released → faster ripening
Common Misconception: "Negative" feedback isn't bad — it's essential for stability! "Positive" feedback isn't always good — it must eventually be stopped by an outside factor or the system would spiral out of control.
AP Exam Tip: Negative feedback is FAR more common in biology because it maintains homeostasis. Positive feedback is used for specific events that need to happen quickly and completely (like blood clotting or childbirth).
4.5

Cell Cycle

The cell cycle is the ordered sequence of events that a cell goes through from one division to the next. It consists of Interphase (growth) and M Phase (division).

The Cell Cycle G₁ Growth S DNA Replication G₂ Prep for division M Mitosis INTERPHASE (G₁ + S + G₂) ~90% of cycle G₁ G₁ Checkpoint (Restriction Point) G₂ G₂ Checkpoint M M Checkpoint (Spindle)
G₁ Phase S Phase G₂ Phase M Phase (Mitosis)
Cell Cycle Phases in Detail

G₁ Phase (Gap 1)

~40% of cell cycle
  • Cell grows in size
  • Produces proteins and organelles
  • Carries out normal functions
  • Prepares for DNA replication
G₁ Checkpoint: Is DNA damaged? Is cell big enough?

S Phase (Synthesis)

~40% of cell cycle
  • DNA replication occurs
  • Each chromosome duplicated → sister chromatids
  • Centrosomes replicate
  • Histone proteins synthesized

G₂ Phase (Gap 2)

~10% of cell cycle
  • More growth and protein synthesis
  • Prepares for mitosis
  • Organelles replicate
  • DNA checked for errors
G₂ Checkpoint: Is all DNA replicated? Any damage?

M Phase (Mitosis + Cytokinesis)

~10% of cell cycle
  • Mitosis: Division of nucleus
  • Cytokinesis: Division of cytoplasm
  • Results in 2 identical daughter cells
M Checkpoint: Are all chromosomes attached to spindle?
Stages of Mitosis (PMAT)
Prophase
Chromatin condenses
Nuclear envelope breaks
→
Metaphase
Chromosomes align
at metaphase plate
→
Anaphase
Sister chromatids
pulled apart
→
Telophase
Nuclear envelopes
reform; cytokinesis
Memory Trick - PMAT: Prophase, Metaphase, Anaphase, Telophase. Or remember: "Please Make Another Taco" or "Pigs Make Awful Tutors"!
4.6

Regulation of Cell Cycle

The cell cycle is tightly controlled by checkpoints and regulatory proteins. When this regulation fails, it can lead to cancer.

Key Regulatory Molecules
Cyclins

Regulatory proteins whose levels fluctuate (cycle) during the cell cycle

Must bind to Cdks to activate them

Cdks (Cyclin-Dependent Kinases)

Kinases that are always present but only active when bound to cyclin

Phosphorylate target proteins to drive cell cycle

Cyclin-Cdk Complex Drives Cell Cycle Cdk (inactive) + Cyclin Cyclin Cdk (ACTIVE) Phosphorylates target proteins Cyclin degraded after use
Cyclins are made and destroyed in a cycle. When cyclin levels rise, they bind to Cdk and activate it. Once the phase is complete, the cyclin is degraded.
The Three Main Checkpoints
Checkpoint Location What Is Checked What Happens If Failed
G₁ Checkpoint
(Restriction Point)		 End of G₁ • Cell size adequate?
• Nutrients available?
• DNA damage?
• Growth signals present?		 Cell enters G₀ (quiescent state) or undergoes apoptosis
G₂ Checkpoint End of G₂ • DNA fully replicated?
• DNA damage repaired?
• Cell large enough?		 Cell cycle arrests; DNA repair attempted
M Checkpoint
(Spindle Checkpoint)		 During metaphase • All chromosomes attached to spindle fibers?
• Proper tension at kinetochores?		 Anaphase delayed until all chromosomes attached
Cancer: When Cell Cycle Control Fails

Cancer results from mutations in genes that control the cell cycle, leading to uncontrolled cell division.

Proto-oncogenes → Oncogenes
Proto-oncogenes: Normal genes that promote cell division (like the "gas pedal").

When mutated: Become oncogenes — overactive, constantly signal cell to divide.

Example: Ras gene (involved in growth signaling)

Tumor Suppressor Genes
Normal function: Stop cell division or trigger apoptosis (like the "brake pedal").

When mutated: Lose function — can't stop abnormal cells from dividing.

Example: p53 ("guardian of the genome"), Rb

Key Concept - p53: The p53 protein is mutated in about 50% of all cancers. It normally detects DNA damage and either halts the cell cycle for repair OR triggers apoptosis (cell death). Without functional p53, damaged cells continue to divide.
Summary: Gas Pedal vs. Brake
Gene Type Normal Function Effect of Mutation Cancer Analogy
Proto-oncogene Promotes cell division Gain of function (overactive) Stuck gas pedal 🚗💨
Tumor Suppressor Inhibits cell division Loss of function (inactive) No brakes 🚗❌
AP Exam Tip: Cancer typically requires mutations in multiple genes — usually both oncogenes and tumor suppressors — before it develops. This is why cancer is more common in older individuals who have accumulated more mutations over time.
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