Biology Quiz: Find the Incorrect Statement
Read each question and the statements below it. Click on the ONE statement you believe is INCORRECT. The explanation will appear after you click an option. If you choose correctly, you’ll earn a point.
Score: 0
State the location within or outside a eukaryotic cell where each of the following stages of aerobic respiration occurs: Glycolysis, Link reaction, Krebs cycle, Oxidative phosphorylation.
Click the INCORRECT location statement:
- 1. Oxidative phosphorylation: Inner mitochondrial membrane (cristae).
- 2. Glycolysis: Mitochondrial matrix.
- 3. Krebs cycle: Mitochondrial matrix.
- 4. Glycolysis: Cytoplasm (cytosol).
- 5. Link reaction: Mitochondrial matrix.
Reason Incorrect (#2): Glycolysis, the initial breakdown of glucose to pyruvate, occurs in the cytoplasm (or cytosol) of the cell (#4 is correct). The subsequent stages – Link reaction (#5), Krebs cycle (#3), and Oxidative phosphorylation (#1) – all take place within the mitochondrion (matrix or inner membrane).
Explain why ATP synthesis by oxidative phosphorylation stops in anaerobic conditions (absence of oxygen).
Click the INCORRECT statement explaining the stoppage:
- 1. Electron carriers (like NADH, FADH₂) cannot pass electrons to the ETC and therefore remain reduced; NAD⁺ and FAD are not regenerated.
- 2. Without oxygen, the Krebs cycle accelerates significantly to compensate for the lack of ATP, quickly depleting acetyl-CoA.
- 3. Oxygen serves as the crucial final electron acceptor at the end of the electron transport chain (ETC).
- 4. Consequently, the pumping of protons (H⁺ ions) from the matrix to the intermembrane space by the ETC complexes ceases.
- 5. Without oxygen to accept electrons, the entire electron transport chain backs up and stops functioning.
- 6. The proton gradient (proton motive force) across the inner mitochondrial membrane dissipates or cannot be established/maintained.
- 7. Without the flow of protons back through ATP synthase driven by the gradient, ATP synthesis via chemiosmosis stops.
Reason Incorrect (#2): In anaerobic conditions, oxygen (#3) is unavailable to accept electrons, causing the ETC to halt (#5). This leads to an accumulation of reduced electron carriers (NADH, FADH₂) because they cannot be re-oxidized (#1). The lack of regenerated NAD⁺ and FAD inhibits the Krebs cycle and Link reaction; they do not accelerate (#2 is incorrect). This stoppage prevents proton pumping (#4), dissipates the proton gradient (#6), and halts ATP synthesis by ATP synthase (#7).
Some cancer cells rely heavily on lactate fermentation even when oxygen is present. Explain how inhibiting the enzyme that catalyses the final step… (pyruvate to lactate) would reduce ATP production in these cells.
Click the INCORRECT statement in the explanation:
- 1. Glycolysis, the main ATP source in these cells, requires a constant supply of NAD⁺ to continue operating.
- 2. Inhibiting lactate dehydrogenase prevents the conversion of pyruvate to lactate.
- 3. Since glycolysis produces ATP via substrate-level phosphorylation, slowing or stopping glycolysis directly reduces the cell’s ATP production.
- 4. Inhibiting lactate dehydrogenase directly blocks the activity of ATP synthase in the mitochondria.
- 5. The conversion of pyruvate to lactate (fermentation) is essential for regenerating NAD⁺ from NADH produced during glycolysis. Inhibiting this step prevents NAD⁺ regeneration.
Reason Incorrect (#4): The purpose of lactate fermentation in these cells is primarily to regenerate NAD⁺ from NADH (#5), which is essential for glycolysis (#1) to continue. Inhibiting lactate dehydrogenase (#2) prevents this NAD⁺ regeneration. Since glycolysis is the main source of ATP (#3), inhibiting it reduces ATP supply. Lactate dehydrogenase inhibition affects glycolysis indirectly by starving it of NAD⁺; it does not directly block ATP synthase (#4), which is involved in oxidative phosphorylation (a separate pathway).
Identify one similarity and one difference between paracrine cell signalling (local diffusion) and endocrine cell signalling (hormones in blood).
Click the INCORRECT statement:
- 1. Difference: Endocrine signals (hormones) typically travel long distances via the bloodstream to reach target cells throughout the body; paracrine signals diffuse only over short distances to affect nearby cells.
- 2. Similarity: Both signalling pathways primarily utilize lipid-soluble signalling molecules that can easily diffuse across cell membranes.
- 3. Similarity: Both involve a signalling molecule (ligand) being released (secreted) by a signalling cell and binding to specific receptors on target cells to elicit a response.
Reason Incorrect (#2): Both paracrine and endocrine signalling involve secreted ligands binding to target cell receptors (#3 is correct), but they differ significantly in the distance travelled (#1 is correct). While some hormones and local mediators are lipid-soluble (like steroids or prostaglandins), many others are water-soluble peptides, proteins, or amino acid derivatives (like insulin, growth factors, neurotransmitters). Therefore, it’s incorrect to state that both pathways *primarily* use lipid-soluble molecules (#2). The nature of the signalling molecule varies widely in both systems.
Explain why a neurotransmitter such as acetylcholine (ACh) could be described as a paracrine signalling molecule.
Click the INCORRECT explanation:
- 1. ACh travels long distances within the bloodstream to coordinate responses in multiple organs simultaneously.
- 2. ACh acts specifically on receptors located on the immediately adjacent postsynaptic cell membrane.
- 3. ACh is released by a presynaptic neurone and diffuses across the very short distance (nanometers) of the synaptic cleft to reach its target.
Reason Incorrect (#1): Paracrine signalling involves local action over short distances. Acetylcholine functions as a neurotransmitter by diffusing across the synaptic cleft, a very short gap, to act on the adjacent postsynaptic cell (#2, #3 are correct). This local action fits the definition of paracrine signalling (or more specifically, synaptic signalling, which is a subtype of paracrine). Hormones travel long distances via the bloodstream (#1), which describes endocrine signalling, not the action of ACh at a synapse.
Experiments investigated a signalling molecule released by muscle cells after palmitate exposure… Results: Control ≈ 1.0; Expt A (medium) ≈ 1.5; Expt B (boiled medium) ≈ 2.6; Expt C (lipid part) ≈ 1.5. Outline conclusions.
Click the INCORRECT conclusion based on the results:
- 1. Conclusion: The signalling molecule is likely lipid-soluble or associated with lipids, as activity similar to the whole medium was recovered in the lipid fraction (Expt C ≈ 1.5, similar to Expt A ≈ 1.5).
- 2. Conclusion: The signalling molecule is likely a protein, as boiling significantly increased its activity (Expt B ≈ 2.6 compared to Expt A ≈ 1.5).
- 3. Conclusion: Palmitate-exposed muscle cells release a signalling molecule into the medium that induces stress gene expression in recipient cells (Expt A shows higher expression than Control).
- 4. Conclusion: The signalling molecule appears to be heat-stable (not easily denatured by boiling), as boiling the medium did not reduce its signalling effect (Expt B shows activity ≥ Expt A).
Reason Incorrect (#2): Boiling typically denatures proteins, causing them to lose their structure and function. The result from Experiment B (boiled medium) shows that the activity *increased* or at least was not destroyed by boiling, compared to the unboiled medium in Experiment A. This indicates the signalling molecule is heat-stable (#4 is correct) and therefore unlikely to be a typical protein (#2 is incorrect). The molecule might be a lipid (#1 is plausible given Expt C) or another heat-stable small molecule. Expt A vs Control confirms a signal is released (#3 is correct).
If stress gene expression inhibits protein translation in developing muscle cells, suggest three ways the structure of these cells might differ from normal muscle cells.
Click the structural difference LEAST likely to result directly from inhibited protein translation:
- 1. Fewer and/or smaller sarcomeres (the basic contractile units containing actin and myosin).
- 2. Lower abundance of actin and myosin protein filaments within the cytoplasm.
- 3. Fewer mitochondria, as mitochondrial biogenesis requires synthesis of numerous proteins encoded by both nuclear and mitochondrial DNA.
- 4. An increased number of ribosomes attached to the endoplasmic reticulum to compensate for the inhibition.
- 5. Fewer and/or smaller myofibrils (the bundles of actin and myosin filaments that make up muscle fibers).
- 6. Reduced amounts of regulatory proteins like troponin and tropomyosin associated with the contractile filaments.
Reason Incorrect (#4): Inhibited protein translation means the cell’s machinery for making proteins (ribosomes) is less active or blocked. This would lead to a reduced synthesis of muscle-specific proteins like actin, myosin, troponin, tropomyosin (#1, #2, #5, #6) and potentially fewer mitochondria if protein import is affected (#3). It is highly unlikely that the cell would respond by increasing the number of ribosomes (#4); reduced protein synthesis generally leads to reduced ribosome biogenesis over time, not an increase.
Describe the mechanism by which stomata open in response to sunlight.
Click the statement describing an event associated with CLOSURE, not opening:
- 1. Potassium ions (K⁺) move out of the guard cells, causing water potential inside to rise and water to follow by osmosis, leading to flaccidity.
- 2. Light (specifically blue light) activates proton pumps (H⁺-ATPases) in the guard cell plasma membrane, actively pumping H⁺ ions out of the cells using ATP.
- 3. The accumulation of K⁺ ions (and associated anions like malate) inside the guard cells significantly lowers (makes more negative) the water potential within these cells.
- 4. Water enters the guard cells from surrounding epidermal cells via osmosis, moving down the water potential gradient (from higher potential outside to lower potential inside).
- 5. Potassium ions (K⁺) move into the guard cells through specific ion channels, driven down the electrochemical gradient established by the proton pumps.
- 6. The influx of water increases the turgor pressure of the guard cells, causing them to bend or bow outwards (due to differential thickening of their cell walls), thereby opening the stomatal pore between them.
Reason Incorrect (#1): Stomatal opening is driven by an increase in guard cell turgor. This occurs when K⁺ ions move *into* the guard cells (#5), lowering the internal water potential (#3), causing water to enter by osmosis (#4), increasing turgor and making the cells bow outwards (#6). Light activates proton pumps to initiate this process (#2). Statement #1 describes the efflux (movement *out*) of K⁺, which leads to water loss, loss of turgor (flaccidity), and stomatal *closure*.
A graph shows that as ABA concentration increases from near 0 to ~250 µmol m⁻³, stomatal conductance decreases steeply (from >2.0 to <0.5 mol m⁻² s⁻¹). Above 250 µmol m⁻³ ABA, conductance remains very low. Describe this relationship.
Click the INCORRECT description of the relationship:
- 1. At higher ABA concentrations (significantly above 250 µmol m⁻³), further substantial increases in ABA concentration cause a proportional, steep increase in stomatal conductance.
- 2. There is a clear negative correlation between ABA concentration and stomatal conductance: as ABA levels rise, conductance generally falls.
- 3. The relationship is non-linear; the effect of ABA is most pronounced at lower concentrations, causing a steep decrease in conductance initially.
- 4. At high ABA concentrations, stomatal conductance reaches a minimum low level, and further increases in ABA have minimal additional effect (saturation effect).
Reason Incorrect (#1): The description clearly states that as ABA concentration increases, stomatal conductance decreases (#2, #3). Furthermore, above ~250 µmol m⁻³, conductance remains very low with little further change (#4). Statement #1 incorrectly suggests that at high ABA levels, conductance would increase steeply and proportionally, which contradicts the observed saturation/minimal effect at high concentrations and the overall negative correlation.
Suggest explanations for the relationship where increasing ABA concentration decreases stomatal conductance.
Click the INCORRECT statement describing ABA’s mechanism for closing stomata:
- 1. ABA binds to specific receptor proteins on the guard cell plasma membrane (or possibly inside the cell), triggering an intracellular signalling cascade, often involving second messengers like calcium ions (Ca²⁺) and reactive oxygen species.
- 2. The signalling cascade leads to the opening of anion channels and K⁺ efflux channels, causing the efflux (movement out) of potassium ions (K⁺) and anions (like Cl⁻, malate²⁻) from the guard cells.
- 3. The loss of solutes increases (makes less negative) the water potential inside the guard cells relative to the surrounding cells.
- 4. ABA binding directly activates the H⁺-ATPase proton pumps in the guard cell membrane, leading to K⁺ influx and increased turgor.
- 5. Water leaves the guard cells by osmosis, moving down the water potential gradient (from higher potential inside to lower potential outside), causing the cells to lose turgor and become flaccid.
- 6. The loss of turgor causes the guard cells to straighten, closing the stomatal pore between them, thus reducing conductance. ABA is often produced in response to drought stress, signalling the need to conserve water.
Reason Incorrect (#4): Abscisic acid (ABA) induces stomatal closure. Its signalling pathway (#1) leads to the efflux (exit) of ions like K⁺ (#2), raising the internal water potential (#3) and causing water to leave by osmosis (#5). This results in loss of turgor and closure (#6). Activation of proton pumps and subsequent K⁺ influx (#4) is the mechanism that drives stomatal *opening*, which ABA signalling inhibits or reverses.
State where transcription factors bind on DNA to cause an increase in the rate of transcription.
Click the INCORRECT binding site for activating transcription factors:
- 1. Ribosome binding site (e.g., Shine-Dalgarno sequence in prokaryotes).
- 2. Terminator sequence.
- 3. Promoter region (often close to the transcription start site) or enhancer regions (which can be distant).
- 4. Start codon (AUG on mRNA).
Reason Incorrect (#1, #2, #4): Transcription factors are proteins that bind to specific DNA sequences to regulate the rate of transcription. Activating transcription factors typically bind to promoter elements or enhancer sequences (#3 is correct) near or far from the gene, helping to recruit RNA polymerase. Ribosome binding sites (#1) and start codons (#4) are features of mRNA involved in initiating translation, not transcription factor binding sites on DNA. Terminator sequences (#2) signal the end of transcription.
Explain how the North American signal crayfish could have evolved resistance to crayfish plague.
Click the statement that represents an incorrect mechanism of evolution:
- 1. Inheritance: Resistant crayfish that survived the plague passed the alleles conferring resistance to their offspring.
- 2. Selection Pressure: Exposure to the crayfish plague pathogen acted as a strong environmental pressure favouring resistant individuals.
- 3. Variation: Within the original crayfish population, random mutations likely generated genetic variation, with some individuals happening to possess alleles providing some level of resistance.
- 4. Directed Mutation: Individual crayfish that were exposed to the plague developed the necessary resistance mutations specifically in response to the need to survive.
- 5. Change in Allele Frequency: Over many generations of exposure and differential survival, the frequency of the resistance alleles increased significantly within the population.
- 6. Differential Survival/Reproduction: Crayfish with pre-existing resistance alleles were more likely to survive infection and reproduce compared to susceptible individuals.
Reason Incorrect (#4): Evolution by natural selection acts on existing variation within a population (#3). Mutations arise randomly, not directed by the organism’s needs or environmental pressures. The crayfish plague acted as a selection pressure (#2), favoring individuals that, by chance, already possessed resistance alleles (#6). These individuals survived and reproduced, passing on the resistance alleles (#1), leading to an increase in their frequency over time (#5). The idea of mutations arising specifically because they are needed (#4) is Lamarckian and not consistent with modern evolutionary synthesis.
Outline and explain the three main temperature steps that occur in one cycle of the polymerase chain reaction (PCR).
Click the statement describing the WRONG action for the Annealing step:
- 1. Annealing (e.g., 50–65°C): Heat-stable DNA polymerase actively binds to the template DNA and begins synthesizing new strands from available nucleotides.
- 2. Denaturation (e.g., 90–98°C): High temperature breaks the hydrogen bonds holding the two strands of the target DNA double helix together, separating them into single strands.
- 3. Extension/Elongation (e.g., 68–75°C, often 72°C): The temperature is raised to the optimal level for the heat-stable DNA polymerase (like Taq polymerase) to synthesize new complementary DNA strands, starting from the primers.
- 4. Annealing (e.g., 50–65°C): The temperature is lowered sufficiently to allow the short, single-stranded DNA primers to bind (anneal) specifically to their complementary sequences on the separated template strands.
Reason Incorrect (#1): The three main steps are Denaturation (#2), Annealing (#4), and Extension (#3). The Annealing step specifically involves lowering the temperature to allow the primers to bind to the template DNA strands (#4). DNA synthesis by the polymerase (#1 describes this) occurs during the subsequent Extension step (#3) at a typically higher temperature optimized for the polymerase activity.
Suggest how researchers identify suitable unique DNA sequences for designing PCR primers specific to a target species like A. pallipes.
Click the LEAST effective or INCORRECT strategy:
- 1. By randomly synthesizing large numbers of short DNA primer sequences and testing each pair empirically until one successfully amplifies DNA only from A. pallipes samples.
- 2. By comparing available DNA sequence data (e.g., from genomic databases) of the target species (A. pallipes) with sequences from closely related species and non-target species using bioinformatics alignment tools.
- 3. By targeting highly conserved DNA regions, such as ribosomal RNA genes, that are known to be identical across all crayfish species and most crustaceans.
- 4. By sequencing parts of the genome (e.g., mitochondrial DNA or specific nuclear genes) from multiple individuals of A. pallipes and comparing these to sequences from other species expected to be in the environment, looking for regions unique to A. pallipes.
Reason Incorrect (#3 and #1): To achieve species-specificity, primers must target DNA sequences that are unique to the target species (A. pallipes) or at least significantly different from those in closely related species (#2, #4 describe this strategy). Targeting highly conserved regions (#3) would likely lead to amplification of DNA from multiple species, defeating the goal of specificity. Random synthesis and testing (#1) is extremely inefficient and impractical compared to bioinformatic approaches using available sequence data. Let’s choose #3 as incorrect because it directly contradicts the goal of specificity.
Standard qPCR curves show fluorescence increasing over cycles. Curves starting with higher DNA amounts cross a set threshold at earlier cycles. Four standards (A, B, C, D) cross the threshold progressively later. Which curve represents the highest starting concentration?
Click the curve representing the HIGHEST starting concentration:
Reason Incorrect (#1, #3, #4): In quantitative PCR (qPCR), the cycle number at which the fluorescence signal crosses a defined threshold (Ct value) is inversely related to the starting amount of target DNA. A higher starting concentration means fewer cycles are needed to reach the threshold. Since the curves cross the threshold in the order A, B, C, D (with A being earliest and D being latest), curve A represents the highest starting concentration.
In a qPCR experiment, DNA from an eDNA sample reached threshold fluorescence at cycle 28. Standard curve C reached threshold at cycle 25. Given that DNA doubles each cycle, calculate how many times lower the starting concentration of the eDNA sample was compared to standard C.
Click the INCORRECT calculation or result:
- 1. 6 times lower (based on 2 multiplied by the difference in cycles: 2 * (28 – 25) = 6).
- 2. 9 times lower (based on squaring the difference in cycles: (28 – 25)² = 3² = 9).
- 3. 3 times lower (based directly on the difference in cycles: 28 – 25 = 3).
- 4. 8 times lower (since each cycle represents a doubling, a 3-cycle difference corresponds to 2³ = 8-fold difference).
Reason Incorrect (#1, #2, #3): PCR amplification is exponential, with the amount of DNA ideally doubling each cycle. A difference of 3 cycles (28 – 25 = 3) between the sample and the standard means the sample started with 2³ (2 to the power of 3) times less DNA. 2³ = 2 × 2 × 2 = 8. Therefore, the eDNA sample concentration was 8 times lower than standard C (#4 is correct). Options #1, #2, and #3 use incorrect mathematical operations.
To create genetically modified bacteria expressing GFP, what component (vector) is typically taken up by the bacteria, and what two essential genetic elements must this component contain besides the GFP gene itself?
Click the option that includes an INCORRECT component or lacks an essential element for expression:
- 1. Vector: Chromosome fragment. Element 1: GFP gene. Element 2: Terminator sequence.
- 2. Vector: Plasmid. Element 1: GFP gene. Element 2: Suitable promoter sequence.
- 3. Vector: Plasmid. Element 1: Promoter sequence. Element 2: Selectable marker (e.g., antibiotic resistance). (Note: assumes GFP gene is also present implicitly for expression context)
- 4. Vector: Ribosome. Element 1: GFP mRNA. Element 2: Promoter sequence.
Reason Incorrect (#1 and #4): Genetic modification of bacteria usually involves introducing a plasmid vector (#2, #3 are plausible vector choices). Chromosome fragments (#1) are generally not stable vectors. Ribosomes (#4) are cellular machinery for translation, not vectors for introducing genes. For the GFP gene to be expressed, the vector must contain the GFP gene itself and a promoter sequence (#2) upstream of it to initiate transcription by the bacterial RNA polymerase. While selectable markers (#3) and terminators are important for plasmid construction and function, the promoter is essential specifically for expressing the inserted gene. Option #1 uses the wrong vector type and lists a terminator but misses the essential promoter. Option #4 uses the wrong vector and molecule type (mRNA instead of DNA gene). Let’s select #1 as incorrect.
Suggest why the gene for GFP is sometimes transferred along with another desired gene in genetic engineering.
Click the INCORRECT reason for using GFP:
- 1. GFP provides strong resistance to common antibiotics, allowing easy selection of transformed cells on antibiotic plates.
- 2. GFP acts as a visual reporter or marker gene; its fluorescence allows researchers to easily identify cells or organisms that have successfully taken up the plasmid (and thus likely the desired gene) by simply observing them under appropriate light.
- 3. GFP encodes an essential chaperone protein required for the correct folding and expression of the co-transferred desired gene’s protein product.
- 4. The bright fluorescence of the GFP protein directly interacts with and enhances the activity or stability of the protein product from the desired gene.
Reason Incorrect (#1, #3, #4): Green Fluorescent Protein (GFP) functions as a reporter gene because its expression results in a visible fluorescent signal (#2 is correct). This allows researchers to track transformation success or gene expression patterns non-invasively. GFP itself does not confer antibiotic resistance (#1); separate antibiotic resistance genes are used for selection. GFP is not a chaperone protein (#3) nor does it typically interact with or enhance the function of other proteins (#4); its role is purely as a marker.
Name areas A (outside the thylakoid) and B (inside the thylakoid) within the chloroplast.
Click the INCORRECT identification:
- 1. A: Intermembrane space, B: Stroma
- 2. A: Cytoplasm, B: Matrix
- 3. A: Stroma, B: Thylakoid lumen / Thylakoid space
- 4. A: Thylakoid lumen, B: Stroma
Reason Incorrect (#1, #2, #4): In a chloroplast, the thylakoids are internal membrane sacs. The fluid-filled space surrounding the thylakoids but enclosed by the chloroplast’s inner membrane is the stroma (A). The space inside a thylakoid sac is the thylakoid lumen or thylakoid space (B). Therefore, option #3 correctly identifies A=Stroma and B=Thylakoid lumen. Options #1, #2, and #4 incorrectly assign these labels or use terms related to mitochondria (matrix) or the whole cell (cytoplasm).
Name the specific biochemical process involving PSI, electron carriers C, and ATP synthase E that produces ATP using light energy but does not involve PSII. Name the protein labelled E.
Click the INCORRECT process or protein identification:
- 1. Process: Calvin cycle. E: Rubisco.
- 2. Process: Cyclic photophosphorylation. E: ATP synthase / ATP synthetase.
- 3. Process: Non-cyclic photophosphorylation. E: NADP reductase.
- 4. Process: Chemiosmosis. E: Proton pump.
Reason Incorrect (#1, #3, #4): The pathway described – involving only Photosystem I (PSI), electron carriers, and ATP synthesis without PSII or NADPH production – is specifically called cyclic photophosphorylation. The enzyme complex responsible for synthesizing ATP using the proton gradient generated during this process is ATP synthase (also called ATP synthetase). Therefore, option #2 is correct. The Calvin cycle (#1) uses ATP and NADPH but doesn’t produce ATP this way. Non-cyclic photophosphorylation (#3) involves both PSI and PSII and produces both ATP and NADPH. Chemiosmosis (#4) is the mechanism by which ATP synthase works, but ‘proton pump’ is not the name for E (ATP synthase).
During non-cyclic photophosphorylation, a reduced hydrogen carrier (labelled D) is produced. Identify product D and describe its specific role in the Calvin cycle.
Click the INCORRECT identity or role for product D:
- 1. Identity of D: FADH₂. Role: Donates electrons to regenerate RuBP in the final stage of the cycle.
- 2. Identity of D: Reduced NADP (NADPH). Role: Provides reducing power (high-energy electrons and H⁺) used to reduce glycerate-3-phosphate (GP) to triose phosphate (TP) during the reduction phase of the cycle.
- 3. Identity of D: NADH. Role: Used directly by ATP synthase to produce ATP required for carbon fixation in the stroma.
- 4. Identity of D: ATP. Role: Directly provides the energy required for the initial carbon fixation step catalysed by RuBisCO.
Reason Incorrect (#1, #3, #4): The reduced hydrogen carrier produced during the light-dependent reactions (specifically non-cyclic photophosphorylation) and used in the Calvin cycle is NADPH (reduced Nicotinamide Adenine Dinucleotide Phosphate) (#2 correctly identifies it). Its role is to provide the electrons (reducing power) needed to convert glycerate-3-phosphate (GP) into triose phosphate (TP). FADH₂ and NADH (#1, #3) are primarily involved in cellular respiration. ATP (#4) is also produced during photophosphorylation and provides energy for the Calvin cycle (both for the reduction of GP and the regeneration of RuBP), but it is not the reduced hydrogen carrier itself.
Data (MJ m⁻² yr⁻¹): Tropical forest ≈ 38, Temperate forest ≈ 24, Snow forest ≈ 15. Describe these results and suggest how limiting factors explain the differences.
Click the INCORRECT description or explanation:
- 1. Description: Net primary productivity (indicative of energy transfer) is highest in snow forests and lowest in tropical forests, likely due to adaptation to cold.
- 2. Description: Energy transfer through photosynthesis decreases significantly from tropical regions towards higher latitudes (temperate and snow forests). Explanation: Factors like lower average annual temperature and/or reduced light intensity and duration at higher latitudes limit the overall rate of photosynthesis compared to the consistently warm and high-light conditions in the tropics.
- 3. Description: All three forest types exhibit very similar rates of energy transfer per unit area per year. Explanation: This is because atmospheric CO₂ concentration, the primary substrate, is relatively uniform globally.
Reason Incorrect (#1 and #3): The data clearly shows a trend of decreasing energy transfer (net primary productivity) from tropical (highest, ~38) to temperate (~24) to snow forests (lowest, ~15). Therefore, statement #1 (claiming snow forest is highest) and statement #3 (claiming rates are similar) are incorrect descriptions of the results. The explanation in #2 correctly identifies likely limiting factors (temperature, light) that cause this decrease at higher latitudes.
Data (MJ m⁻² yr⁻¹): Grasslands (Tropical ≈ 12, Temperate ≈ 9) and Desert (<5) show lower energy transfer rates than forests. Suggest reasons for this.
Click the LEAST likely or INCORRECT reason:
- 1. Reason: Forests typically have a much higher density of plant life and greater total leaf area index (biomass) per unit ground area compared to most grasslands and especially deserts, allowing them to intercept more sunlight.
- 2. Reason: Water availability is often a major limiting factor in deserts and many grasslands, restricting photosynthesis because plants close stomata to conserve water, limiting CO₂ uptake.
- 3. Reason: Deserts generally experience optimal temperatures and consistent sunlight throughout the year, allowing maximum photosynthetic rates whenever water is present.
- 4. Reason: Nutrient availability (e.g., nitrogen, phosphorus) in the soil might be lower or more limiting in certain grassland or desert ecosystems compared to productive forests.
Reason Incorrect (#3): While deserts often have high sunlight intensity, they are characterized by extreme temperatures (often too high for optimal enzyme function during the day) and severe water scarcity (#2). These factors strongly limit photosynthesis, making statement #3 (claiming optimal temperatures and maximum rates) incorrect. Lower biomass (#1) and potential nutrient limitations (#4) also contribute to lower productivity compared to forests.
Homologous chromosomes share the same genes at the same loci. State one other structural feature shared by a pair of homologous chromosomes visible during meiosis.
Click the feature NOT shared by homologous chromosomes:
- 1. Same number of mitochondria associated with their centromeres.
- 2. Same overall size / length.
- 3. Identical alleles for every gene along their length.
- 4. Same characteristic banding pattern when subjected to specific staining techniques (e.g., G-banding).
- 5. Same shape, determined by the position of the centromere (e.g., both metacentric, both acrocentric).
Reason Incorrect (#1 and #3): Homologous chromosomes are pairs (one inherited from each parent) that carry the same genes in the same order (loci). Structurally, they are typically the same size (#2), have the same centromere position/shape (#5), and show the same banding pattern (#4). However, they do not necessarily carry the same alleles for each gene (#3 is incorrect); they can carry different versions (e.g., one dominant, one recessive). Mitochondria are organelles in the cytoplasm and are not structurally associated with chromosomes in this way (#1 is incorrect).
Albinism (lack of pigment) can be caused by homozygous recessive mutations of the TYR gene, which codes for the enzyme tyrosinase involved in melanin production. Explain why a person homozygous recessive for TYR shows albinism.
Click the INCORRECT statement in the explanation:
- 1. The mutated recessive alleles code for an overactive form of the tyrosinase enzyme, which rapidly consumes all melanin precursors, preventing pigment formation.
- 2. Being homozygous recessive means the individual inherited two copies of a mutated allele for the TYR gene (one from each parent).
- 3. The enzyme tyrosinase plays a critical, early role in the biochemical pathway that synthesizes melanin pigments.
- 4. These mutated alleles typically result in the production of a non-functional or inactive tyrosinase enzyme, or potentially no enzyme at all.
- 5. Without functional tyrosinase enzyme activity, the melanin synthesis pathway is blocked, and melanin pigment cannot be produced, resulting in the characteristic lack of pigmentation (albinism).
Reason Incorrect (#1): Albinism is a condition resulting from the *lack* of melanin pigment. This is typically caused by mutations that lead to a non-functional or inactive enzyme (tyrosinase) required for melanin synthesis (#4, #5). A homozygous recessive individual has two such mutated alleles (#2). An overactive enzyme (#1) would theoretically lead to *more* pigment production, not less, and is not the cause of albinism related to TYR gene mutations.
In rabbits, black fur (B) is dominant to brown (b), but allele F is required for pigment production (ff results in white fur). Complete the genetic diagram for a cross between two black rabbits heterozygous for both genes (BbFf × BbFf) and state the ratio of offspring phenotypes.
Click the INCORRECT statement regarding the cross or its outcome:
- 1. Gametes that can be produced by each BbFf parent: BF, Bf, bF, bf.
- 2. Parental Genotypes for the cross: BbFf × BbFf.
- 3. Offspring Phenotype Ratio expected: 9 Black : 3 Brown : 4 White.
- 4. Offspring Phenotype Ratio expected: 9 Black : 7 White (where brown and white phenotypes are indistinguishable).
- 5. Punnett square analysis yields expected genotype proportions of 9 B_F_ : 3 bbF_ : 3 B_ff : 1 bbff. Phenotypes: B_F_ = Black; bbF_ = Brown; B_ff = White; bbff = White.
Reason Incorrect (#4): This scenario describes recessive epistasis, where the homozygous recessive genotype at one locus (ff) masks the expression of alleles at another locus (B/b). A standard dihybrid cross between two double heterozygotes (BbFf x BbFf) (#1, #2 are correct) results in genotype proportions 9 B_F_ : 3 bbF_ : 3 B_ff : 1 bbff (#5 describes this). The corresponding phenotypes are 9 Black (B_F_), 3 Brown (bbF_), and (3+1=) 4 White (B_ff and bbff). Therefore, the correct phenotypic ratio is 9 Black : 3 Brown : 4 White (#3 is correct). A 9:7 ratio (#4 is incorrect) arises in other types of epistatic interactions where both double recessive (ff) and the presence of the homozygous recessive at the first locus (bbF_) result in the same phenotype, which isn’t the case here as brown (bbF_) is distinct from white (ff).
Data: Cattle (0.08 mutations/Mb/yr, 20yr lifespan); Ferret (0.20, 8yr); Horse (0.05, 30yr); Human (0.02, 75yr); Mouse (0.28, 3.6yr). Describe the relationship shown.
Click the statement that INCORRECTLY describes the relationship:
- 1. There is no clear or discernible relationship between the somatic mutation rate per year and the maximum lifespan across these species.
- 2. There is a strong positive correlation: species with higher mutation rates per year tend to exhibit significantly longer lifespans.
- 3. There appears to be a negative correlation or inverse relationship: species with higher mutation rates per megabase per year generally have shorter lifespans (e.g., compare Mouse/Ferret to Human/Horse).
Reason Incorrect (#1 and #2): Observing the data reveals a pattern: species with high mutation rates per year (Mouse 0.28, Ferret 0.20) have short lifespans (3.6yr, 8yr), while species with low mutation rates per year (Human 0.02, Horse 0.05) have long lifespans (75yr, 30yr). Cattle fall in between. This indicates a clear negative (or inverse) correlation (#3 is correct). Therefore, statements suggesting no relationship (#1) or a positive correlation (#2) are incorrect descriptions of the trend shown in the data.
Using the relationship described (inverse correlation between mutation rate/year and lifespan), explain how these species might differ in their potential rate of adaptation if environmental selection pressures change.
Click the INCORRECT explanation regarding adaptation potential:
- 1. Species with lower mutation rates per year (like humans and horses) are likely to adapt much faster because their genomes are more stable, allowing beneficial adaptations to persist without being disrupted by new mutations.
- 2. All species likely adapt at roughly the same rate over geological time, as the intensity of the selection pressure is the primary determinant, outweighing differences in mutation rate or lifespan.
- 3. Species with higher mutation rates per year and shorter generation times (often associated with shorter lifespans, like mice) generate more genetic variation per unit of time and undergo more generations of selection in that time, giving them a greater potential capacity to adapt more quickly to changing environments.
- 4. Species with longer lifespans (like horses and humans) have a greater potential for adaptation because individuals have more time within their own lifetime to develop physiological or learned adaptations to environmental changes.
Reason Incorrect (#1, #2, #4): Evolutionary adaptation occurs over generations through changes in allele frequencies driven by natural selection acting on heritable variation. The rate depends on the amount of variation generated (mutation rate) and how quickly selection can act (related to generation time). Species with higher mutation rates and shorter generation times (#3 is correct) generally have a higher *potential* rate of genetic adaptation because they produce more variants and experience more rounds of selection per unit time. Lower mutation rates (#1) provide less raw material for selection. While individual physiological adaptation occurs (#4), it’s not evolutionary adaptation, which involves genetic change across generations. Assuming rates are the same (#2) ignores the impact of mutation and generation time.
Compare the typical timescales needed for selective breeding versus genetic engineering to significantly increase the frequency of a rare desirable allele in a cattle population. Give a reason.
Click the INCORRECT comparison or reason:
- 1. Comparison: Both methods generally require a similar number of generations and therefore take roughly the same amount of calendar time to achieve significant allele frequency changes in long-generation animals like cattle.
- 2. Comparison: Genetic engineering techniques generally allow for much faster increases in allele frequency compared to the much slower process of traditional selective breeding.
- 3. Reason for Selective Breeding Speed: Progress is gradual, requiring repeated cycles of identifying superior individuals, mating them, and evaluating offspring over many generations, limited by the animal’s natural reproductive cycle length.
- 4. Reason for Genetic Engineering Speed: Allows for direct introduction or selection of the allele, potentially combined with advanced reproductive technologies (like cloning, marker-assisted selection with IVF, sperm/egg sorting) to rapidly multiply desired genotypes, potentially achieving large changes in 1-2 generations.
- 5. Comparison: Selective breeding is generally considered faster because it utilizes natural mating processes, whereas genetic engineering involves complex and time-consuming laboratory procedures before application.
Reason Incorrect (#1 and #5): Genetic engineering offers the potential for much more rapid genetic change than traditional selective breeding, especially for traits influenced by single genes or when combined with reproductive technologies (#2, #4 are correct). Selective breeding is inherently slow in species with long generation times like cattle, requiring many years to significantly alter allele frequencies through repeated selection cycles (#3 is correct). While GE involves lab work, its ability to directly target genes or rapidly propagate genotypes bypasses the generational bottleneck of conventional breeding, making it potentially much faster overall (#1, #5 are incorrect).
State two features of dairy cattle that could potentially be improved using genetic engineering.
Click the feature LEAST likely or impossible to be a target for genetic engineering in dairy cattle:
- 1. Milk yield / overall quantity of milk produced per lactation.
- 2. Ability to perform photosynthesis using sunlight and CO₂.
- 3. Resistance to specific diseases (e.g., mastitis, respiratory infections).
- 4. Milk quality attributes (e.g., higher protein content, altered fat composition, reduced allergens).
- 5. Development of functional wings for flight capability.
Reason Incorrect (#2 and #5): Genetic engineering in livestock focuses on enhancing traits related to agricultural productivity, animal health, and product quality (#1, #3, #4 are valid examples). Introducing entirely new, complex biological systems like photosynthesis (#2, characteristic of plants/algae) or flight (#5) involves altering potentially hundreds or thousands of genes and developmental pathways, making it currently impossible and certainly not a practical goal for dairy cattle improvement.
Outline three roles of the International Union for Conservation of Nature (IUCN) in the conservation of species.
Click the role NOT primarily carried out by the IUCN itself:
- 1. Assessing the global conservation status of species and assigning them to risk categories (e.g., Critically Endangered, Vulnerable) published in the IUCN Red List of Threatened Species.
- 2. Directly managing and enforcing international treaties and regulations governing the trade in endangered species and their products.
- 3. Providing scientific information, expertise, and policy advice to governments, international conventions (like CITES, CBD), and conservation organizations.
- 4. Raising public awareness about biodiversity loss and conservation issues through publications, campaigns, and educational materials.
- 5. Supporting and facilitating on-the-ground conservation action through its network of members, commissions, and partnerships.
Reason Incorrect (#2): The IUCN plays crucial roles in assessing risk (#1), providing scientific advice (#3), raising awareness (#4), and supporting conservation actions (#5). However, the direct regulation and enforcement of international trade in endangered species is the primary mandate of CITES (Convention on International Trade in Endangered Species of Wild Fauna and Flora), an international agreement between governments. While IUCN provides scientific assessments that inform CITES listings, it does not manage or enforce the trade regulations itself.
Grizzly bears and polar bears… can interbreed… to produce fertile ‘pizzly bear’ offspring. Discuss whether they should be classified as separate species, referring to three different species concepts.
Click the statement making an INCORRECT or overly definitive conclusion based on the species concept described:
- 1. Morphological Species Concept: Based on their significant, distinct physical differences (morphology) adapted to different environments, they would likely be classified as separate species.
- 2. Biological Species Concept (BSC): Because they can interbreed in nature and produce fertile offspring, indicating a lack of complete reproductive isolation, they might be considered the same species (or subspecies) under a strict BSC definition.
- 3. Ecological Species Concept: Given that they occupy distinct ecological niches defined by their different habitats (arctic ice vs temperate forests/tundra) and primary diets (seals vs varied omnivorous), they would likely be classified as separate species.
- 4. Phylogenetic Species Concept: Because they undoubtedly share a relatively recent common ancestor, they must definitively be classified as the same species under this concept.
Reason Incorrect (#4): The Phylogenetic Species Concept (PSC) defines species based on unique, shared evolutionary history, often identified as the smallest diagnosable cluster of individuals with a parental pattern of ancestry and descent (monophyly). While polar bears and grizzly bears share a common ancestor, the PSC requires assessing whether they form distinct, diagnosable evolutionary lineages based on genetic data. Recent divergence and ongoing hybridization can make PSC classification complex. Stating they *must definitively* be the same species just because they share a common ancestor (#4) is an oversimplification and misapplication of the concept; the degree and diagnosability of divergence are key. The other options correctly apply their respective concepts to the scenario.
Calculate Simpson’s Index of Diversity (D) for a spectacled bear population using D = 1 – Σ(n/N)², given the sum of the (n/N)² values [Simpson’s Dominance Index] is 0.272.
Click the INCORRECT calculation or value for D:
- 1. D = 0.272 (This is the Dominance Index, not the Diversity Index)
- 2. D = 1 / 0.272 ≈ 3.68 (This calculates the reciprocal of the Dominance Index, sometimes used as another diversity measure, but not the one defined by the formula D = 1 – Σ(n/N)²)
- 3. D = 1 – 0.272 = 0.728
- 4. D = 1 + 0.272 = 1.272 (Incorrect formula application)
Reason Incorrect (#1, #2, #4): The formula provided for Simpson’s Index of Diversity is D = 1 – Σ(n/N)². The value of the summation term Σ(n/N)² (which represents Simpson’s Dominance Index) is given as 0.272. Plugging this into the formula gives D = 1 – 0.272 = 0.728 (#3 is correct). Options #1, #2, and #4 represent either the dominance index itself, its reciprocal, or an incorrect calculation.
The calculated Simpson’s Index of Diversity (D) value for the disturbed habitat population was 0.728, while the D value for an undisturbed population was 0.833. Explain what the difference in D values indicates about the bears’ diet in the two habitats.
Click the INCORRECT interpretation:
- 1. The higher D value (0.833) found in the undisturbed habitat indicates a lower dietary diversity, meaning the bears consumed fewer types of food or relied heavily on one type.
- 2. The lower D value (0.728) found in the disturbed habitat indicates a higher dietary diversity compared to the undisturbed habitat.
- 3. The higher D value (0.833) for the undisturbed population indicates greater dietary diversity (the bears consumed a wider variety of food items, and/or consumed them in more even proportions) compared to the bears in the disturbed habitat (D=0.728).
- 4. The D values directly represent the total number of individual bears sampled in each habitat.
Reason Incorrect (#1, #2, #4): Simpson’s Index of Diversity (D), calculated as 1 – Dominance Index, ranges from 0 (low diversity) to almost 1 (high diversity). A higher value indicates greater diversity. Therefore, the undisturbed habitat with D=0.833 has higher dietary diversity than the disturbed habitat with D=0.728 (#3 is correct). Statements #1 and #2 incorrectly interpret the meaning of higher/lower D values. Statement #4 is incorrect as D measures diversity (related to richness and evenness of food types), not population size.
State two differences between discontinuous variation and continuous variation, other than their genetic basis.
Click the INCORRECT comparison:
- 1. Phenotypic Categories: Discontinuous variation falls into distinct, separate categories (e.g., blood groups A, B, AB, O); Continuous variation shows a range or spectrum of phenotypes with intermediates (e.g., height).
- 2. Environmental Influence: Phenotypes in discontinuous variation are usually minimally affected by environmental factors; phenotypes in continuous variation are often significantly influenced by the environment.
- 3. Genetic Basis: Discontinuous variation typically involves multiple genes (polygenic); Continuous variation typically involves a single gene with major effects.
- 4. Graphical Representation: Discontinuous variation data is often plotted using bar charts; Continuous variation data is typically plotted using histograms, often approximating a normal distribution curve.
- 5. Environmental Influence: Continuous variation phenotypes are largely determined by genetics with little environmental input; Discontinuous variation phenotypes are heavily modified by environmental conditions.
Reason Incorrect (#5 and #3): Statement #5 incorrectly reverses the typical environmental influence; continuous variation is often strongly affected by environment, while discontinuous is less so (#2 is correct). The question asked to exclude genetic basis, but statement #3 incorrectly describes the genetic basis; discontinuous usually involves one or few major genes, while continuous involves multiple genes (polygenic) interacting with the environment. Distinct categories vs range (#1) and graphical representation (#4) are correct differences.
Harlequin ladybirds show several distinct colour patterns (e.g., conspicua, spectabilis, succinea) in populations. Suggest the genetic basis for this type of variation.
Click the INCORRECT description of the genetic basis:
- 1. It represents continuous variation, likely controlled by the cumulative effects of many genes (polygenic inheritance), each with a small additive effect, interacting with environmental factors.
- 2. It represents discontinuous variation, where individuals fall into distinct phenotypic categories. This pattern is likely controlled by one or a few major genes, possibly involving multiple alleles at a single locus or epistatic interactions between loci.
- 3. It results purely from environmental factors experienced during development (e.g., diet, temperature) affecting pigment synthesis, with no genetic component involved.
Reason Incorrect (#1 and #3): The existence of several distinct, named colour patterns indicates discontinuous variation, where phenotypes fall into separate categories (#2 is correct). This pattern is typically under the control of a limited number of genes with significant effects, potentially involving complexities like multiple alleles or epistasis. Continuous variation (#1) would result in a smooth range of colours or patterns, not distinct types. While environment can sometimes influence phenotype, distinct heritable patterns like these strongly imply a primary genetic basis, making purely environmental control (#3) unlikely.
Adult ladybird body size shows continuous variation (5mm to 8mm). State two environmental factors during the larval stage that might affect the final adult body size.
Click the factor LEAST likely to be an environmental influence on larval growth affecting adult size:
- 1. Availability, quantity, and nutritional quality of the food supply accessible to the larva during its growth period.
- 2. The specific allele(s) inherited by the larva for the gene controlling its adult colour pattern (e.g., conspicua vs succinea allele).
- 3. Ambient temperature experienced during larval development, affecting metabolic rate and growth duration.
- 4. The genetically determined number of spots that will appear on the adult ladybird’s elytra.
Reason Incorrect (#2 and #4): Continuous variation traits like body size are influenced by both genetics and environment. Environmental factors experienced during the growth phase (larval stage) are crucial. These include resource availability (food, #1) and physical conditions like temperature (#3). Genetic factors like the alleles for colour pattern (#2) or spot number (#4) are inherited traits and do not represent environmental influences on growth, although there could potentially be pleiotropic genetic links (one gene affecting multiple traits) which is different from direct environmental effect.
Describe how the binding of sucrose to a chemoreceptor cell leads to the generation of an action potential in the associated sensory neurone.
Click the INCORRECT statement in the sequence:
- 1. Sucrose molecules bind to specific transmembrane receptor proteins located on the membrane of the chemoreceptor cell.
- 2. This binding triggers a conformational change in the receptor, leading to the opening of specific ion channels (often permeable to Na⁺ or Ca²⁺) in the chemoreceptor cell membrane.
- 3. The influx of positive ions causes a depolarisation (making the inside less negative) of the chemoreceptor cell membrane, known as a receptor potential.
- 4. If this receptor potential is strong enough to reach a threshold level, it triggers the release of neurotransmitter molecules from the chemoreceptor cell into the synaptic cleft separating it from the sensory neurone.
- 5. Neurotransmitter molecules diffuse across the cleft and bind to specific ligand-gated ion channels (often Na⁺ channels) on the postsynaptic membrane of the sensory neurone, causing them to open.
- 6. The resulting influx of Na⁺ into the sensory neurone causes a depolarisation (postsynaptic potential). If this depolarisation reaches the threshold potential for the sensory neurone, it triggers the opening of voltage-gated sodium channels, initiating an action potential that propagates along the sensory axon.
- 7. Sucrose binding directly triggers a full, propagating action potential within the chemoreceptor cell itself, which then transmits directly to the sensory neurone.
Reason Incorrect (#7): Most sensory receptor cells (like chemoreceptors for taste) respond to stimuli with graded receptor potentials (#3), not full action potentials. It is the release of neurotransmitter triggered by this receptor potential (#4) that leads to a postsynaptic potential in the associated sensory neuron (#6). Only if this postsynaptic potential reaches the threshold of the sensory neuron will an action potential be generated and propagated along its axon. Statement #7 incorrectly describes the receptor cell itself firing the action potential.