UPHESC Assistant Professor Genetics & Plant Breeding PYQs

Concept: A single crossover inside the loop of a paracentric inversion heterozygote gives a dicentric chromatid (forming an anaphase I bridge) and an acentric fragment.

1. In a pericentric inversion the centromere lies within the loop, so crossover gives duplication–deficiency chromatids but no dicentric bridge.
2. Bridge + fragment at anaphase I is the cytological signature of paracentric inversion.

Short trick: PARA = centromere outside loop → bridge + fragment.

Concept: The Ph1 (pairing homoeologous) gene on the long arm of chromosome 5B (Riley & Chapman; Sears & Okamoto, 1958) restricts pairing to true homologues, giving diploid-like meiosis.

1. Without 5B (nullisomic 5B) homoeologous chromosomes of A, B, D genomes pair.
2. ph1b mutant is used to transfer alien genes into wheat.
3. There is no 'C' genome in bread wheat (AABBDD).

Short trick: Pairing homoeologous = Ph1 on 5BL.

Concept: Genetic load (H. J. Muller, 1950) is the reduction in mean fitness of a population, relative to the optimum genotype, caused by deleterious alleles (mutational, segregational load etc.).

1. L = (W_max − W̄)/W_max.
2. Drift (genetic/random) is chance change in gene frequency in small populations.
3. Genetic gain is response to selection – an improvement, not a decrease.

Short trick: Deleterious alleles = a 'load' on fitness.

Concept: Linkage disequilibrium D = f(AB)·f(ab) − f(Ab)·f(aB), the difference between products of coupling and repulsion gamete frequencies.

1. D = 0 → linkage equilibrium (alleles associate at random).
2. D decays each generation by a factor (1 − r) under random mating.
3. LD is the basis of association mapping.

Short trick: D = coupling product − repulsion product; D ≠ 0 = disequilibrium.

Concept: Nilsson-Ehle (1909, wheat kernel colour) and East (1916, Nicotiana corolla length) proposed the multiple factor hypothesis: quantitative traits are controlled by many genes, each with small, similar and additive (cumulative) effect.

1. Multiple alleles = more than two alleles of one locus (e.g. ABO).
2. Dominance and overdominance hypotheses explain heterosis.

Short trick: Many small additive genes = multiple factors (Nilsson-Ehle).

Concept: p(A) = (2 × AA + Aa) / (2 × N).

1. Number of A alleles = 2(360) + 480 = 1200.
2. Total alleles = 2 × 1000 = 2000.
3. p = 1200/2000 = 0.6 (q = 0.4); check: p² = 0.36, 2pq = 0.48, q² = 0.16 – population is in H-W equilibrium.

Short trick: p = frequency(AA) + ½ frequency(Aa) = 0.36 + 0.24 = 0.6.

Concept: Comstock and Robinson (1948, 1952) developed biparental progeny / North Carolina mating designs to estimate additive and dominance variance.

1. Biparental mating in early segregating generations was later advocated to break linkages (Jensen's diallel selective mating is related).
2. Kempthorne – line × tester (1957); Hayman – diallel analysis.

Short trick: Biparental progenies / NC designs → Comstock & Robinson.

Concept: The graphical (Vr–Wr) and component analysis of diallel crosses was developed by Jinks and Hayman (1953; Hayman 1954, Jinks 1954).

1. It estimates D, H₁, H₂, F, h², E and gives the average degree of dominance.
2. Griffing (1956) gave the combining-ability approach.

Short trick: Diallel: Hayman–Jinks (genetic components), Griffing (combining ability).

Concept: In NCD-I each male is mated to a different set of females (nested). σ²_males = ¼σ²_A and σ²_{females/males} = ¼σ²_A + ¼σ²_D (F = 0, no epistasis).

1. So both additive and dominance variances are estimated (σ²_D with poorer precision).
2. NCD-II (factorial) also gives σ²_A and σ²_D; NCD-III gives σ²_A, σ²_D and average degree of dominance.

Short trick: NC-I: males → A; females-within-males → A + D.

Concept: MAGIC (Multi-parent Advanced Generation Inter-Cross) populations are developed by intercrossing 4, 8 or 16 founder parents and then selfing to RILs.

1. NIL, RIL and F_2:3 are bi-parental (two-parent) mapping populations.
2. NAM (nested association mapping) is another multiparent design.

Short trick: MAGIC = Many parents.

Concept: Selection differential S = mean of selected – population mean = i·σ_P, where i (k) = selection intensity in standard units and σ_P = phenotypic standard deviation.

1. Genetic advance GA = k·σ_P·h² (Johnson et al., 1955).
2. At 5% selection k = 2.06.

Short trick: S = k × σ_P; GA = k σ_P h².

Concept: Kearsey and Jinks (1968) extended North Carolina Design III by adding the F₁ as a third tester: each F₂ (or other) individual is crossed to P₁, P₂ and F₁.

1. NCD-III uses only the two parents as testers.
2. The TTC additionally detects epistasis and gives unbiased D and H.

Short trick: NCD III + F₁ tester = Triple Test Cross.

Concept: The full six-parameter model (Hayman 1958; Jinks & Jones) has m, d, h, i, j, l. The five-parameter model m, d, h, i, j omits l – the dominance × dominance interaction.

1. d = additive, h = dominance, i = additive × additive, j = additive × dominance, l = dominance × dominance.
2. Same sign of h and l → complementary epistasis; opposite → duplicate.

Short trick: Drop the last letter 'l' (D × D) → five parameters.

Concept: In Hayman's diallel analysis, $(H_1/D{)}^{1/2}$ is the mean degree of dominance.

1. = 0 → no dominance.
2. between 0 and 1 → partial dominance.
3. = 1 → complete dominance.
4. > 1 → overdominance.

Short trick: Ratio 1 = complete; >1 = over; <1 = partial.

Concept: Simple interval mapping, using a pair of flanking markers and maximum-likelihood LOD scores, was proposed by Eric Lander and David Botstein (Genetics, 1989) – implemented in MAPMAKER/QTL.

1. Single-marker analysis came earlier (Sax 1923; Soller et al.).
2. Composite interval mapping: Zeng (1993, 1994); Jansen (1993).

Short trick: 1989 Lander–Botstein → SIM; 1994 Zeng → CIM.

Concept: Non-allelic interaction (epistasis) in generation-mean analysis is detected by scaling tests.

1. Mather's (1949) individual scaling tests A, B, C, D (e.g. A = 2B₁ − P₁ − F₁): if any scale differs significantly from zero, epistasis is present – so 'Scaling test' (D) is correct.
2. The joint scaling test (Cavalli, 1952) fits the additive–dominance model (m, [d], [h]) to all generation means together and tests the fit by χ²; a significant χ² shows that non-allelic interaction is present – so 'Joint scaling test' (B) also determines the presence or absence of epistasis.
3. Test cross (genotype/linkage testing) and scale effect (a property of the measurement scale) do not.
4. Since two options (B and D) both fit the description, the question has no single answer as printed.

Short trick: Both Mather's A-B-C-D scales and Cavalli's joint scaling χ² test for epistasis.

Concept: Additive and additive × additive gene effects are fixable – they are retained in homozygous lines after selfing, so such heterosis can be fixed in pure lines.

1. Dominance, additive × dominance and dominance × dominance effects depend on heterozygosity and decline on inbreeding – non-fixable.
2. Hence hybrids are needed when heterosis is due to dominance/overdominance.

Short trick: Fixable = A + A×A; non-fixable = anything with 'D'.

Concept: In a double cross (A × B) × (C × D) the related inbreds are placed in the same single cross, so that the two single crosses are genetically unrelated and give maximum heterosis.

1. The performance of the double cross itself is predicted from the four non-parental single crosses (Jenkins, 1934).
2. Parental single-cross performance and inbred yield are used for seed-production convenience, not to fix the order.

Short trick: Related inbreds together; unrelated single crosses across.

Concept: Second-cycle inbreds (from crosses among elite first-cycle inbreds, i.e. pedigree selection) are mainly superior in their own (per se) vigour and yield.

1. Their combining ability and hybrid performance are generally not much better than those of the first-cycle lines, because both cycles sample similar germplasm.
2. Improved per se yield makes seed production of hybrids cheaper.

Short trick: 2nd-cycle inbreds = stronger lines themselves, not necessarily better combiners.

Concept: Single-gene heterosis (Hull 1945: heterozygote a₁a₂ superior to both homozygotes at one locus) is the overdominance explanation – a genetic basis of heterosis.

1. Genetic theories: dominance (Davenport; Bruce; Jones), overdominance/single-gene heterosis (Shull, East, Hull), epistasis.
2. Biochemical/physiological theories deal with enzymes, growth rates, mitochondrial complementation.

Short trick: Single gene → genetic (overdominance) theory.