AP Biology Exam Review Notes

Long FRQ 1: Microbial Fermentation – Experimental Design

Scenario: Scientists are bioengineering microbes to increase ethanol production through anaerobic fermentation by modifying a bacterial gene involved in fermentation.

(a) Experimental Design:

Objective: To test if overexpression of a gene encoding pyruvate decarboxylase increases ethanol production in bacteria.

Procedure:

Genetic Modification: Genetically modify bacteria to overexpress the pyruvate decarboxylase gene using plasmids or other genetic tools to enhance gene expression.

Control vs. Experimental Groups: Grow both modified and unmodified bacteria in parallel to isolate the effect of the genetic modification.

Environment: Use identical anaerobic, glucose-rich environments for both groups; control temperature, pH, and nutrient availability.

Duration: Allow a fixed time for growth (e.g., 24 hours) to ensure sufficient ethanol production for accurate measurement.

Measurement: Measure ethanol concentrations using gas chromatography to compare ethanol output between the two groups. Use replicates to ensure statistical validity.

(b) Null Hypothesis and Control Group:

Null Hypothesis: Overexpression of the pyruvate decarboxylase gene will have no significant effect on ethanol production.

Control Group: Unmodified bacteria grown under the same conditions as the experimental group. This baseline allows for comparison against the modified bacteria.

(c) Prediction and Justification:

Prediction: Ethanol production will increase in the genetically modified bacteria.

Justification: Overexpression of pyruvate decarboxylase enhances the conversion of pyruvate to ethanol, accelerating fermentation and generating more ATP under anaerobic conditions. This is because more enzyme is available to catalyze the reaction.

(d) Additional Genetic or Environmental Change:

Change: Inhibit the enzyme NADH dehydrogenase, which is part of aerobic respiration, using a specific inhibitor.

Justification: Inhibiting NADH dehydrogenase prevents the cell from using oxygen for energy, forcing it to rely more on fermentation, thus increasing ethanol production. This ensures that the metabolic pathway is directed towards ethanol production.

Long FRQ 2: Antifungal Drug – Membrane Structure

(a) Drug Target:

The antifungal drug affects fungal cells but not human cells because human cells contain cholesterol in their membranes, not ergosterol. Ergosterol is unique to fungal membranes.

The drug specifically binds to ergosterol, disrupting fungal membranes without affecting human cells, making it selectively toxic to fungi. This is due to the specific molecular interaction between the drug and ergosterol.

(b) Effect of Disrupting Ergosterol:

Disrupting ergosterol increases membrane permeability.

This causes essential ions and molecules to leak out of the fungal cell, leading to a loss of homeostasis, reduced energy production, and eventual cell death. The cell can no longer maintain its internal environment.

(c) Effect of Mutation Eliminating Ergosterol Synthesis:

The fungus would become resistant to the drug, as there would be no ergosterol for the drug to bind. The drug will not have its intended target.

However, the mutation may reduce membrane fluidity and impair nutrient transport, resulting in slower growth and reduced fitness in environments without the drug. This creates a trade-off between drug resistance and normal function.

(d) Graph of Survival Rates:

X-axis: Drug concentration (increasing from left to right).

Y-axis: Percent survival.

Wild-type line: Drops steeply as concentration increases, showing sensitivity to the drug.

Mutant line:

Declines more gradually, indicating resistance. This shows the protective effect of the mutation.

May start at a lower baseline to reflect reduced fitness of the mutant strain even without the drug.

Short FRQ 1: Epigenetics & Cell Cycle

Scenario: The p53 gene in a cancer cell is methylated instead of acetylated at its promoter region.

(a) p53 Expression:

No, p53 will not be expressed.

Methylation condenses the chromatin and prevents RNA polymerase from binding, blocking transcription. The promoter becomes inaccessible.

(b) Normal Role of p53:

p53 detects DNA damage and halts the cell cycle to allow repair.

If damage is severe, it initiates apoptosis to prevent the damaged cell from dividing through programmed cell death.

(c) Consequence of p53 Silencing:

The cell will continue dividing despite DNA damage, increasing the likelihood of mutation accumulation and cancer development. This loss of control leads to genomic instability.

(d) Changes in Transcription and Translation:

Methylation prevents transcription of the p53 gene, so no mRNA is produced. The gene is effectively silenced.

Without mRNA, translation cannot occur, and no p53 protein is synthesized. The protein required for cell cycle control is absent.

Short FRQ 2: Pedigree & Meiosis

(a) Inheritance of Recessive Alleles:

During meiosis I, homologous chromosomes separate, each carrying one allele.

Each parent can pass on the recessive allele in a gamete, following the law of segregation.

If a child inherits the recessive allele from both parents, they will be affected, showing the recessive phenotype.

(b) Punnett Square:

Mating: Aa × Aa

Genotypes:

25% AA (unaffected)

50% Aa (carrier)

25% aa (affected)

(c) Probability of Affected Child:

25% or 1 in 4.

(d) Crossing Over:

Crossing over shuffles alleles between homologous chromosomes, increasing genetic diversity. This occurs during prophase I of meiosis.

However, it does not change the Mendelian probabilities for a single-gene trait like this autosomal recessive disorder. The overall probabilities remain the same.

Short FRQ 3: Cladograms & Amino Acids

(a) Amino Acid Similarity:

Species with more similar amino acid sequences have fewer differences due to fewer accumulated mutations, indicating a more recent common ancestor. Fewer mutations suggest less time has passed since divergence.

(b) Most Recent Common Ancestor:

The two species with the fewest amino acid differences in cytochrome c likely share the most recent common ancestor, as they have diverged less genetically. Their evolutionary paths are closely related.

(c) Derived Trait:

A derived trait is a new feature shared by all organisms beyond a specific node. It distinguishes one clade from another and indicates a common ancestor that first had the trait. This trait defines the branch.

(d) Additional Mutations:

More mutations would increase genetic distance, potentially moving that species further away from others on the cladogram, suggesting an earlier divergence. The position on the cladogram reflects the degree of genetic change.

Short FRQ 4: Photosynthesis & Invasive Species

(a) Light-Dependent Reactions:

Light-dependent reactions occur in the thylakoids and use sunlight to split water, releasing oxygen and producing ATP and NADPH. These reactions convert light energy into chemical energy.

These energy carriers are then used in the Calvin cycle to fix carbon into glucose, storing the energy in sugar molecules.

(b) Effect of Invasive Plants:

Invasive plants may block sunlight, reducing the rate of light-dependent reactions in native plants. This shading reduces the energy available for photosynthesis.

This lowers ATP and NADPH production and decreases glucose synthesis, affecting the overall productivity of the native plants.

(c) Effect on Ecosystem:

Invasive species often outcompete native species for resources, reducing biodiversity. The ecosystem becomes less diverse.

This can disrupt food webs and make the ecosystem less stable and more vulnerable to collapse, impacting ecosystem services.

(d) Testing Method:

Set up two plots: one with invasive plants and one without.

Measure CO₂ uptake in native plants using sensors to assess photosynthesis rates, ensuring light, water, and temperature are controlled. This measures the photosynthetic activity.

Concept: Glycolysis, Fermentation, and Anaerobic Respiration

Glycolysis:

First step in breaking down glucose, occurs in the cytoplasm of all cells.

Does not require oxygen.

Products:

2 pyruvate molecules

2 ATP (net gain) via substrate-level phosphorylation

2 NADH (from NAD⁺ being reduced)

Fermentation:

Regenerates NAD⁺, essential for glycolysis to continue.

Uses pyruvate as an electron acceptor.

Converts pyruvate into:

Ethanol + CO₂ (yeast and some bacteria)

Lactic acid (human muscle cells and some bacteria)

Does not make additional ATP.

In the FRQ, connect genetic changes to microbes that increase ethanol output by enhancing the fermentation step or redirecting metabolic flow toward ethanol production. This enhances ATP production under anaerobic conditions.

Concept: Enzyme Function (Active Site, Specificity, Denaturation)

Enzymes:

Proteins that catalyze biological reactions.

Bind to substrates at a specific active site.

Lower the activation energy needed for the reaction.

Highly specific – one enzyme usually works on one type of molecule.

Can be denatured (lose shape and function) by heat, pH, or salinity.

Enzyme-substrate interactions form a temporary complex, positioning molecules for reaction. This facilitates the conversion of substrates to products.

In fermentation, enzymes like pyruvate decarboxylase and alcohol dehydrogenase convert pyruvate into ethanol.

Overexpressing these enzymes means there are more active sites available, more reactions can happen simultaneously, faster conversion of pyruvate, more ethanol. This increases the rate of ethanol production.

In an FRQ, explain that a genetically modified microbe expressing more fermentation enzymes would increase fermentation rate and ethanol output due to increased catalytic capacity. The increased number of enzymes enhances the reaction rate.

Concept: ATP Generation and NAD⁺ Regeneration

Anaerobic conditions:

ATP is produced only via glycolysis (2 ATP per glucose).

Glycolysis converts NAD⁺ to NADH.

Without oxygen, NADH can’t be oxidized via the electron transport chain.

Fermentation regenerates NAD⁺, using pyruvate as an electron sink.

No NAD⁺ = no glycolysis = no ATP = death. Glycolysis stops without NAD+ regeneration.

Link to FRQ: If you want microbes to make more ethanol (and survive better anaerobically), increasing NAD⁺ regeneration is key. Genetic engineering can help by enhancing the fermentation pathway that does this. This enhances the efficiency of the fermentation process.

Concept: Designing Experiments (Controls, Variables, Hypotheses)

Independent variable: the thing you change – e.g., presence of a gene that increases fermentation enzyme expression.

Dependent variable: the result you measure – e.g., ethanol concentration.

Control group: organisms without the gene modification.

Constants: glucose level, time, temperature, pH, anaerobic conditions ensure consistent results.

Null hypothesis: There will be no difference in ethanol output between modified and unmodified microbes.

Alternative hypothesis: Modified microbes will produce more ethanol due to increased fermentation enzyme activity.

Justification: Connect your prediction to biological logic – increased enzyme levels → faster fermentation → more ethanol → more NAD⁺ regeneration. This provides a rationale for the expected outcome.

Concept: How Genetic Modifications Affect Metabolic Pathways

Genetic modification:

Insert a gene, amplify its expression, or silence another gene. These changes alter enzyme availability.

This changes which enzymes are present and how metabolites are routed.

Example:

Overexpressing pyruvate decarboxylase = more pyruvate is converted to acetaldehyde.

This shifts metabolic flow from the Krebs cycle toward fermentation. The metabolic pathway is redirected.

As a result, ethanol output increases, and aerobic respiration may decrease. This impacts ATP production.

In an FRQ, you must link the gene change to pathway shifts and changes in energy or byproduct output. Use terms like:

“Metabolic flux”

“Resource allocation”

“Redirection of pyruvate metabolism” to explain the changes.

Concept: Membrane Structure – Phospholipids, Sterols (Ergosterol vs. Cholesterol)

Biological membranes are composed of:

A phospholipid bilayer (hydrophobic tails inside, hydrophilic heads outside). This provides the basic structure.

Embedded proteins (channels, pumps, receptors). These carry out specific functions.

Sterols, which help stabilize the membrane. These maintain membrane fluidity.

Cholesterol is the sterol in animal (including human) cells.

Ergosterol is found only in fungal membranes. This is a key difference between fungi and humans.

This biochemical difference is key: antifungal drugs like amphotericin B and azoles selectively bind to ergosterol, poking holes in fungal membranes – but they don’t harm human cells because humans lack ergosterol. The drugs target the unique sterol in fungi.

In the FRQ, you must explain that the antifungal selectively targets fungal membranes due to the presence of ergosterol – a structure-function relationship that enables specificity. This specificity is crucial for the drug's effectiveness.

Concept: Selective Permeability and Membrane Transport

The cell membrane is selectively permeable, meaning it controls what enters and exits. This is essential for maintaining cell function.

Maintains ion gradients (e.g., Na⁺, K⁺).

Nutrient uptake.

Waste removal.

pH and osmotic balance.

Disrupting sterols like ergosterol compromises membrane integrity:

Large gaps form.

Ions leak out (K⁺, H⁺).

Water enters → lysis.

Proteins and small molecules drift across inappropriately. The membrane loses its barrier function.

Result: the fungal cell loses homeostasis and dies. Homeostasis disruption leads to cell death.

This is a perfect FRQ opportunity to describe how structure (ergosterol) supports function (permeability) and how disrupting it leads to cell death. The loss of membrane integrity is fatal.

Concept: Effects of Membrane Disruption on Homeostasis

Homeostasis: maintaining a stable internal environment.

In fungi, ergosterol helps:

Keep the membrane fluid but not too leaky. This maintains optimal membrane properties.

Anchor membrane proteins. This ensures proper protein function.

Maintain correct permeability. This controls the flow of substances in and out of the cell.

Without ergosterol:

The membrane becomes unstable.

Ions leak out.

ATP gradients collapse. Energy production is compromised.

The cell may burst or shrink. Osmotic balance is disrupted.

Enzymes stop working due to pH or ion imbalance. Metabolic processes are impaired.

Link this to energy: membrane pumps (like H⁺-ATPases) require a stable gradient to produce ATP. If ions leak, the proton gradient collapses, and ATP production stops. ATP production fails due to proton gradient collapse.

Concept: Mutations and Their Impact on Fitness (Trade-offs)

A fungal mutation that eliminates or alters ergosterol prevents the drug from binding, granting resistance. This mutation confers drug resistance.

However, this comes at a cost:

Without ergosterol, the membrane is less functional.

The fungus might grow more slowly. Growth rate decreases.

It might struggle to uptake nutrients or communicate between cells. Nutrient uptake is compromised.

In a drug-free environment, it is outcompeted by the wild-type. The wild-type has a fitness advantage.

This is a classic evolutionary trade-off: increased survival under stress, but reduced performance in normal conditions. There is a trade-off between resistance and fitness.

Use the phrase: “This resistance mutation provides a selective advantage in the presence of the drug but results in a fitness cost in the absence of the drug.” This clearly states the evolutionary trade-off.

Concept: Drug Resistance and Evolutionary Pressures

Ties to natural selection:

Fungal populations have variation in their membrane genes. Genetic variation exists within the population.

When exposed to antifungal drugs, most cells die. The drug acts as a selective pressure.

Any resistant mutant survives → differential survival. Resistant individuals survive and reproduce.

These survivors reproduce → adaptation. The population adapts to the drug.

Real-world example of antibiotic/antifungal resistance, and it’s great to connect it to:

Genetic mutation

Heritability

Environmental pressure

Fitness

Selective pressure

Key terms to use: variation, differential survival, heritable traits, fitness, selective pressure. These terms explain the process of natural selection.

Concept: Interpreting and Drawing Survival Graphs

Common FRQ visuals.

You’re often asked to:

Draw or analyze a graph showing % survival vs. drug concentration.

Here’s what it should look like:

Wild-type fungi: steep drop in survival as drug concentration increases. This shows sensitivity to the drug.

Mutant fungi: higher survival even at high drug doses (shallower curve). This indicates resistance to the drug.

Label your axes:

X-axis: Drug concentration.

Y-axis: Percent survival.

Add a legend or label both curves, and explain: “The resistant strain has increased survival at higher drug concentrations, indicating successful adaptation.” The graph illustrates adaptation through differential survival.

Concept: DNA Methylation and Histone Acetylation (Epigenetics)

Epigenetic modifications change gene expression without changing the DNA sequence. These are heritable changes in gene expression.

DNA methylation = addition of $CH_3$ groups to cytosine bases. This silences genes by tightening chromatin, so RNA polymerase can’t access DNA, and no transcription occurs. Methylation inhibits gene expression.

Histone acetylation = adds acetyl groups to histone tails. This loosens chromatin, opening DNA for transcription, increasing gene expression. Acetylation promotes gene expression.

In the FRQ, if p53 is normally acetylated (active), but becomes methylated (silenced), then it can’t perform its tumor-suppressing function. This sets up conditions for uncontrolled cell division. Silencing p53 impairs its tumor-suppressing function.

Concept: Transcription vs. Translation

Central dogma:

Transcription = DNA → mRNA (in nucleus).

Translation = mRNA → protein (at ribosome).

If transcription is blocked (like through methylation), then:

No mRNA is made. The gene cannot be transcribed.

No translation occurs. Protein synthesis is halted.

No protein (like p53) is synthesized. The protein is absent due to transcriptional block.

In FRQs, be precise: methylation blocks transcription, not translation directly. Methylation’s effect is on transcription.

Concept: p53 and Tumor Suppressor Genes

p53 is a key tumor suppressor protein. It regulates cell cycle and apoptosis.

Roles:

Halts cell cycle at G1/S checkpoint if DNA is damaged. This allows for DNA repair.

Initiates DNA repair or apoptosis if the damage is too great. This prevents propagation of damaged cells.

Without p53:

Cells keep dividing even with DNA damage. There is a loss of cell cycle control.

Mutations accumulate. Genomic instability increases.

Increased risk of cancer. Cancer development is promoted.

In FRQs, explain that epigenetic silencing of p53 leads to unregulated cell cycle progression and potential tumor development. p53 silencing promotes cancer development.

Concept: Cell Cycle Checkpoints (G1/S and G2/M)

Checkpoints are built-in safety systems:

G1/S: checks for DNA damage before replication. Prevents replication of damaged DNA.

G2/M: checks for DNA damage post-replication before mitosis. Prevents division of damaged cells.

p53 works at G1/S. If p53 is nonfunctional, cells with damaged DNA skip repair and enter S phase → mutations get copied. Damaged DNA is replicated, leading to mutation accumulation.

In an FRQ, tie this to how a failure in cell cycle regulation contributes to genomic instability and cancer. Cell cycle failure promotes genomic instability and cancer.

Concept: Apoptosis and Cancer

Apoptosis = programmed cell death. This eliminates damaged cells.

Triggered when:

DNA is too damaged.

Cell is infected or misfolded.

p53 can activate apoptotic genes when damage is severe. p53 triggers apoptosis in severely damaged cells.

Loss of p53:

Prevents apoptosis. Damaged cells survive.

Damaged cells survive, divide. This leads to proliferation of damaged cells.

Leads to tumorigenesis. Tumor formation is promoted.

Use the phrase: “Loss of p53 removes a key control point, allowing damaged cells to bypass apoptosis and continue dividing.” This explains the role of p53 in preventing tumorigenesis.

Concept: Meiosis I and II (Segregation, Independent Assortment)

During meiosis I, homologous chromosomes (carrying different alleles) separate. This reduces chromosome number by half.

During meiosis II, sister chromatids split. This further divides the chromosomes.

Segregation ensures that gametes carry only one allele per gene. This maintains proper chromosome number in offspring.

Independent assortment explains how alleles of different genes are distributed randomly into gametes. This increases genetic variation.

In an FRQ: explain how a child could inherit two recessive alleles (aa) by getting one “a” from each heterozygous (Aa) parent. Both parents are carriers and contribute the recessive allele.

Concept: Punnett Squares and Probability

For Aa × Aa:

25% AA (unaffected).

50% Aa (carrier).

25% aa (affected).

Probability of a child being affected = 25%.

Be sure to:

Draw the square.

Label genotypes.

Explain how you arrive at each %. Show the workings for each probability.

Concept: Autosomal vs. Sex-Linked Inheritance

Autosomal traits: located on chromosomes 1–22.

Sex-linked traits: usually on X chromosome.

For autosomal recessive:

Males and females affected equally.

Carriers show no symptoms.

In an FRQ: state that equal distribution across sexes = autosomal. This helps identify the inheritance pattern.

Concept: Pedigree Analysis Symbols and Genotypes

Circle = female.

Square = male.

Shaded = affected.

Half-shaded = carrier.

Horizontal line = mating.

Vertical line = offspring.

You may be asked to infer genotypes. Practice logic: if two unaffected parents have an affected child → both are carriers (Aa). This is a common pattern in autosomal recessive inheritance.

Concept: Crossing Over and Genetic Variation

Crossing over = exchange of genetic material between homologous chromosomes during prophase I. This increases genetic diversity.

Creates new allele combinations. New combinations of genes arise.

Increases diversity. Genetic diversity is enhanced.

Does NOT affect Mendelian probability of inheriting one gene. The overall probabilities remain predictable.

In an FRQ: clarify that crossing over adds diversity, but inheritance of a single gene like a recessive disorder still follows Punnett predictions. Crossing over does not alter single-gene inheritance probabilities.

Concept: Cladogram Construction and Interpretation

Cladograms are tree diagrams showing evolutionary relationships. Branching patterns indicate evolutionary history.

Each node = common ancestor. This represents a point of divergence.

Organisms grouped together share more traits. Shared traits reflect common ancestry.

In a molecular comparison FRQ, you must:

Count differences in amino acid sequences. Fewer differences indicate closer relationships.

Use fewest differences = closest relationship. Molecular data helps construct cladograms.

Concept: Molecular Evidence of Evolution (Cytochrome c)

Cytochrome c = a conserved protein used to compare species. Its sequence similarity reflects evolutionary relationships.

Fewer amino acid differences = more recent divergence. Less time has passed since speciation.

Example:

Species A and B differ by 3 AAs.

Species A and C differ by 8 AAs.

$\rightarrow$ A and B are more closely related. This is strong molecular homology. A and B share a more recent common ancestor.

Concept: Derived Traits and Nodes on a Phylogenetic Tree

A derived trait is a new feature not present in ancestors. Shared by all members beyond a certain branch point. This trait defines the clade.

In cladograms:

Traits appear at branch points (nodes). New traits arise at nodes.

Later species inherit them. These traits are passed on to subsequent species.

You might be asked to place species or traits correctly on the tree — use trait presence to guide you.The presence/absence of traits helps construct the tree.

Concept: Mutation as a Source of Variation

Mutations change DNA sequences. Mutations drive evolutionary change.

Over time:

Mutations accumulate.

Protein sequences (like cytochrome c) diverge.

These changes reflect evolutionary time.

The more mutations, the greater the molecular distance between species. Molecular distance is an indicator of evolutionary divergence.

Concept: Common Ancestry and Evolutionary Relationships

Closest relatives = species that share the most recent common ancestor. Closer relatives share more recent ancestry.

This is shown by:

Branch proximity on the cladogram indicates close relationships.

Shared derived traits reflect common ancestry.

Smallest number of molecular differences indicates closer relationships.

In an FRQ, you might be asked to interpret evolutionary distance using both the tree and the molecular data. Integrate both types of evidence for a comprehensive analysis.

Concept: Light-Dependent vs. Light-Independent Reactions

Light-dependent reactions (in thylakoid membranes):

Use sunlight to split water (photolysis)

Release $O_2$

Produce ATP and NADPH

Light-independent reactions (Calvin cycle in stroma):

Use ATP/NADPH to fix $CO_2$ into glucose

Know the inputs/outputs and where each happens. Understand the flow of energy and matter through the process.

Concept: Chloroplast Structure and Energy Flow

Chloroplast structure:

Thylakoids = stacked membranes with chlorophyll -> site of light reactions

Stroma = fluid matrix -> site of Calvin cycle

Energy flow: Sunlight -> chlorophyll -> ATP/NADPH -> glucose

You could be asked to trace energy from light to sugar. Understand how energy is captured and stored.

Concept: Limiting Factors in Photosynthesis

Photosynthesis is affected by:

Light intensity

$CO_2$ concentration

Temperature

Each has an optimal range. Too little = slow rate. Too much = saturation or enzyme denaturation. Understand the effect of each factor on photosynthetic rate.

FRQs may ask you to interpret a photosynthesis rate graph with one of these factors manipulated. Analyze the graph to determine the limiting factor.

Concept: Invasive Species and Competitive Exclusion

Invasive species:

Outcompete natives for light, nutrients, space

Reduce photosynthesis in shaded native plants

Can lead to competitive exclusion (native species eliminated). Understand the consequences of competition.

Be ready to describe how this reduces biodiversity.Loss of species diversity is a key effect.

Concept: Biodiversity, Species Richness, and Ecosystem Stability

Biodiversity = variety of species

Species richness = number of different species

Evenness = relative abundance

Ecosystems with high biodiversity are more resilient to changes. Invasive species reduce richness and destabilize ecosystems.A diverse ecosystem is more stable.

Concept: Experimental Design in Ecology (Control vs. Test Plots)

Be able to describe an experiment:

Control plot = no invasive species

Test plot = with invasive species

Keep light, water, $CO_2$ constant. Control environmental variables.

Measure rate of photosynthesis (e.g., $CO2$ uptake or $O2$ production). Measure the dependent variable.

This applies experimental design principles to ecology.Experimental design is crucial for ecological studies.

2. trp Operon & Gene Regulation (Unit 6: Gene Expression & Regulation)

Key Terms

Operon: a cluster of genes under one promoter, controlled by a regulatory sequence.

Repressible operon (e.g., trp): normally on, turned off when the product is abundant.

Inducible operon (e.g., lac): normally off, turned on when a substrate is present.

Mechanism of trp Operon Regulation

No tryptophan: repressor is inactive -> operon is transcribed -> enzymes make tryptophan.

High tryptophan: tryptophan binds repressor -> active repressor binds operator -> transcription blocked.

Applications in FRQs

Predict expression levels based on nutrient conditions.

Analyze effects of mutations (e.g., defective operator = constitutive expression).

Compare with lac operon: lac is catabolic + inducible; trp is anabolic + repressible.

3. Signal Transduction Pathways (Unit 4: Cell Communication)

Core Steps

1. Reception: Ligand binds to a receptor (e.g., G-protein coupled receptor).
2. Transduction: Cascade of proteins (often involving phosphorylation) amplifies the signal.
3. Response: Change in gene expression, enzyme activation, or cell behavior.

Key Concepts

Protein kinases: phosphorylate (activate) downstream targets.

Second messengers (e.g., cAMP, $Ca^{2+}$): amplify the signal inside the cell.

Transcription factors: activated by signaling to turn genes on/off.

FRQ Applications

Predict effects of receptor or kinase mutation.

Explain amplification and specificity.

Relate signaling defects to disease or cell malfunction.

4. Feedback Loops & Homeostasis (Unit 4)

Negative Feedback

Maintains internal balance.

Example: Blood glucose

High glucose -> insulin -> glucose uptake & storage

Low glucose -> glucagon -> glycogen breakdown -> glucose release

Positive Feedback

Amplifies a signal.

Example: Oxytocin during labor -> contractions -> more oxytocin -> more contractions

Disruption Consequences

Type I diabetes: no insulin = constant hyperglycemia

Unchecked positive feedback = dangerous amplification (e.g., cytokine storm)

FRQ Applications

Interpret graphs showing glucose levels or hormone feedback.

Predict the effect of organ damage or hormone dysfunction.

5. Immune System – Adaptive Response (Unit 8)

B and T Cells

B cells: make antibodies, part of humoral immunity

T helper cells: activate B and cytotoxic T cells

Cytotoxic T cells: kill infected cells presenting foreign antigens

Memory cells: enable faster response on re-exposure

Self vs. Non-Self Recognition

MHC proteins identify self

Foreign antigens = immune response

Breakdown = autoimmune disease

FRQ Applications

Predict immune failure (e.g., HIV targets helper T cells)

Compare primary vs. secondary response

Relate to vaccination, immunity, and transplant rejection

6. Nitrogen Cycle (Unit 8: Ecology)

Cycle Stages

1. Fixation: $N2$ -> $NH3$ by bacteria
2. Nitrification: $NH3$ -> $NO2^-$ -> $NO_3^-$
3. Assimilation: $NO_3^-$ absorbed by plants
4. Denitrification: $NO3^-$ -> $N2$ by anaerobic bacteria

Human Impact

Fertilizer overuse -> nitrogen runoff -> eutrophication

Algal blooms deplete oxygen -> aquatic death

FRQ Applications

Draw the cycle with labels

Explain how bacteria enable plant growth

Predict outcomes of pollution or disrupted cycling

7. DNA Replication (Unit 6)

Enzymes Involved

Helicase: unwinds DNA

DNA polymerase: synthesizes new strand (5’ to 3’)

Ligase: joins Okazaki fragments on the lagging strand

Semi-Conservative Replication

Each new DNA molecule = 1 parent strand + 1 new strand

Proven by Meselson-Stahl with isotopic labeling of DNA

FRQ Applications

Predict effects of mutations in enzymes

Explain directionality (why lagging strand is fragmented)

Link replication to mutation and cancer

8. Comparative Anatomy & Evolution (Unit 7)

Hom