(a) Both segments encode Met-Phe-Gln because UUU and UUC both encode Phe. Ribosomes read successive mRNA codons, tRNAs pair anticodons with codons and deliver amino acids, and peptide bonds join the amino acids.

(b) The displayed substitution is synonymous and leaves this peptide segment unchanged, so the proposed amino-acid explanation is unsupported. Activity falls by 6 units, or 60%, but abundance, other sequence regions or experimental conditions could differ. Measure activity per equal amount of purified protein from matched replicated genotypes to separate abundance from activity per molecule.

(a) Aa × Aa gives genotype proportions 1/4 AA, 1/2 Aa and 1/4 aa, with phenotype proportions 3/4 dominant and 1/4 recessive. The expected recessive count is 120 × 1/4 = 30. Actual counts may differ through random fertilisation and survival.

(b) The offspring lane contains an upper larger A fragment and a lower smaller a fragment, supporting Aa under the model. This is consistent with heterozygosity, conditional on reliable amplification and allele assignment. Explain any two suitable controls: known-genotype samples verify allele assignment; a ladder checks size; a no-template tube tests contamination; matched extraction/amplification conditions test comparability. Two well-explained controls suffice.

(a) Frequency rises in every interval from 18% at G0 to 49% at G4, a net increase of 31 percentage points. The plotted pattern is consistent and positive, but the graph alone does not identify its mechanism.

(b) If the phenotype is heritable and improves survival or reproductive success under a shift from pale gravel to dark leaf litter because it involves dark elytra that reduce visual detection, carriers contribute more offspring. The associated allele is then represented more often in the next generation, increasing its frequency over time.

(c) The supplied context states that thirty marked beetles enter from a neighbouring reach carrying the P allele, which is evidence for gene flow. Gene flow can add alleles through migrants, whereas drift changes frequencies by chance most strongly in small populations. Either process can act with selection, so migrant genotypes and effective population size are required.

(d) Track replicated populations and reference sites; genotype random samples each generation; measure the candidate phenotype, survival and reproductive output; estimate effective population size and migration; compare change at the candidate locus with neutral loci and report sampling uncertainty.

(a) The stimulus is that haemolymph trehalose concentration rises. An appropriate sensor detects the deviation. In this organism, metabolic or hormonal signals following carbohydrate sensing coordinate tissue responses that reduce circulating trehalose; any biologically defensible pathway is acceptable and specific hormone names are not required. The resulting response is that trehalose synthesis, transport and use are adjusted to lower the circulating concentration. This opposes the original disturbance so haemolymph trehalose returns towards its regulated range; the response is limited by the organism's tolerance range.

(b) Use a justified non-harmful treatment range from pilot evidence; randomly allocate comparable study units; standardise life stage, acclimation, exposure time and measurement method; use adequate independent replication; and apply organism-appropriate care and biosecurity that uses non-harmful diets, minimises handling and specifies recovery and housing conditions.

(c) The mean response index increases from 20 to 29 and 37 as the disturbance increases. Means from four organisms without individual values, spread or measurement uncertainty cannot show reliability or overlap. The data also do not show whether regulation succeeded or exceeded tolerance limits.

(d) Repeat independent trials with more organisms, record the regulated internal variable and effector response over time, report individual data and confidence intervals, include recovery measurements and predefine the tolerance range. Replicate the study at relevant environmental conditions before generalising.

(a) Influenza A virus is the infectious agent. The stated route is droplet and aerosol transmission: infectious respiratory particles are inhaled and the virus replicates in susceptible respiratory cells; crowding increases effective contacts while ventilation lowers particle exposure. This mechanism is consistent with the supplied context that respiratory particles spread during crowded indoor rehearsals. Infected people shed the newly replicated virus, becoming new sources of infection at rehearsals. This can occur before symptoms develop and cases are recognised. Successive exposure and infection events, followed by incubation and reporting delays, can produce the rising weekly pattern.

(b) Innate barriers, inflammation, complement and phagocytes respond rapidly and non-specifically. Adaptive B lymphocytes produce antigen-specific antibodies, while T lymphocytes provide cell-mediated functions. Clonal expansion takes time during first exposure, and antigen-specific memory B and T cells enable a faster, stronger response to subsequent exposure to the same antigen.

(c) By week 4 the comparison setting has 63 notified cases per 1,000 people and the intervention setting has 31 per 1,000, a rate difference of 32 per 1,000. Both series rise, but the intervention rate grows more slowly with improved ventilation plus vaccination. The denominator-standardised association is consistent with lower transmission risk, not proof that the intervention alone caused it.

(d) The supplied per-1,000 denominator improves comparability, but missing confidence intervals, genomic linkage and individual exposure data limit causal attribution. The intervention population is smaller and participation differs between rooms. Feasibility, equity, privacy, participation, cost and unintended harms should be considered alongside outbreak severity and transmission biology. A decision can be precautionary while evidence is updated.

(e) Continue improved ventilation plus vaccination as a monitored, time-limited measure because the denominator-standardised series is consistent with benefit and the biological mechanism is plausible. Use matched settings or phased introduction, standardised testing, population and person-time denominators, coverage and contact data, pathogen typing where appropriate, adverse-effect and cost monitoring, and confidence intervals. Predefine thresholds for continuation, modification and withdrawal.