Biology • Year 12 • Module 5 • Lesson 13

Sources of Genetic Variation — Meiosis, Crossing Over, Fertilisation, Mutation

Apply the four sources of variation to a sibling-genotype scenario, to a real allele-frequency dataset, to a diagram critique, and to a "sort the source" classification task.

Apply · Data & Reasoning

1. Sort the source — classify each event

For each event in the table, identify which one of the four sources of variation best explains it (crossing over · independent assortment · random fertilisation · mutation) and give a one-sentence justification using lesson terminology. 12 marks (1 source + 2 justification = 3 marks per row × 4 rows; or 1.5 each as marked)

#EventSourceJustification (1 sentence)
1.1 Two non-identical siblings inherit a slightly different mix of grandparents' alleles because their parents' gametes happened to fuse in different combinations.
1.2 A single base in a parent's germ-line DNA changes from G to A, producing a new allele that neither parent previously carried.
1.3 During meiosis in a parent, paired homologous chromosomes physically exchange a segment, producing a recombinant chromosome with both maternal and paternal alleles along its length.
1.4 At metaphase I, the orientation of each homologous pair is independent of every other pair, so each gamete receives a different combination of whole maternal and paternal chromosomes.
Stuck? Use the rule from the lesson Trap callout: only one of the four sources can create a new allele; the other three only rearrange existing alleles.

2. Interpret graph — sibling genotype identity vs number of independently assorting chromosome pairs

The graph below plots the maximum number of genetically distinct gametes a single parent can produce through independent assortment alone, against the haploid number n (number of chromosome pairs). The formula is 2n. The dashed line marks the human value (n = 23). 6 marks

1 10 10² 10³ 10⁴ 10⁵ 10⁶ 10⁷ 10⁸ 1 5 10 15 20 23 Haploid number n (chromosome pairs) Distinct gamete types from independent assortment (2ⁿ, log scale) n=1, 2 gametes n=5, 32 n=10, ≈1×10³ n=15, ≈3×10⁴ n=23 (human), ≈8.4×10⁶

Independent assortment alone, 2n distinct gamete types. Crossing over and mutation are not included in this count.

2.1 Using the graph, estimate the number of distinct gametes a human can produce by independent assortment alone. Show how you read this off the graph. 2 marks

2.2 Explain why the curve is steeper on a log axis at higher n, in terms of what each extra chromosome pair contributes to gamete variety. 2 marks

2.3 The 8.4 million figure ignores crossing over, random fertilisation and mutation. Briefly state how each of those three would change the actual number of possible offspring genotypes a couple can produce. 2 marks

3. Diagram critique — what's wrong with this student's diagram?

A Year 12 student has drawn the diagram below to explain "where genetic variation comes from". There are three biological errors. Identify each error and write the correction. 6 marks (2 per error: 1 identify, 1 correct)

Diagram coming soon

3.1 Error 1: What is wrong?

Correction:

3.2 Error 2: What is wrong?

Correction:

3.3 Error 3: What is wrong?

Correction:

Stuck? Compare this diagram to the lesson's own concept map in Card 5 and the Precision callout in Card 4.

4. Apply to a new scenario — sibling pairs and a brand-new allele

A clinical geneticist sequences three siblings (S1, S2, S3) born to the same two parents (P1, P2). She finds that:

6 marks

4.1 Account for the 99.6% of variation among the siblings — which of the four lesson sources is doing the work, and how? 3 marks

4.2 The geneticist concludes that the G→A change in S2 must be a de novo mutation in a parental germ-line cell. Justify this conclusion using the lesson's distinction between "new allele combinations" and "new alleles". 2 marks

4.3 If S2 went on to reproduce, would this G→A variant be transmissible to S2's children? Justify in one sentence. 1 mark

Stuck? Connect Card 4 (mutation is the only source of new alleles) with Cards 2 and 3 (the other sources reshuffle existing alleles).
Answers — Do not peek before attempting

Q1 — Sort the source (12 marks)

1.1 Random fertilisation. Any one gamete from one parent can fuse with any one gamete from the other parent, producing many possible zygote genotypes — this is what differs from sibling to sibling [3].

1.2 Mutation. A change in DNA base sequence creates a genuinely new allele not present in either parent — only mutation can do this [3].

1.3 Crossing over. Exchange of corresponding segments between paired homologous chromosomes during meiosis produces recombinant chromosomes carrying new combinations of existing alleles [3].

1.4 Independent assortment. Random orientation of homologous pairs at metaphase I distributes whole chromosomes into gametes in different combinations [3].

Q2.1 — Estimate from graph (2 marks)

Read up from n = 23 on the x-axis to the curve; the y-value sits just above the 10⁶ gridline and just below 10⁷, at approximately 8.4 × 10⁶ (about 8 million) distinct gametes [1 estimate + 1 method described].

Q2.2 — Why steeper on log axis at higher n (2 marks)

Each additional chromosome pair doubles the number of distinct gametes (2n), because each pair independently contributes a binary choice [1]. On a log axis the curve is in fact a straight line of constant slope (each unit of n adds a factor of 2), but the absolute gain per extra chromosome rises exponentially — going from n = 22 to 23 adds 4 million extra gamete types where going from 1 to 2 adds only 2 [1].

Q2.3 — Effect of the three other sources (2 marks)

Crossing over multiplies the count further by allowing each chromosome itself to come in many recombinant forms, not just maternal-or-paternal [0.5]. Random fertilisation multiplies the parental gamete counts together (≈ 8.4×10⁶ × 8.4×10⁶ for humans, so ~7×10¹³ zygote types per couple) [0.5]. Mutation contributes extra variation by introducing new alleles not in the existing gamete count at all [1].

Q3 — Diagram critique (6 marks)

3.1 Error 1 ("crossing over creates new alleles"): Crossing over reshuffles existing alleles by exchanging chromosome segments — it does not change DNA base sequence. Correction: redraw the arrow from "crossing over" to "new allele combinations", and have the arrow to "new alleles" come from mutation only. [1 + 1]

3.2 Error 2 (random fertilisation drawn before meiosis): Fertilisation is the fusion of gametes, which can only happen after meiosis has produced those gametes. Correction: redraw the flow so meiosis (with crossing over and independent assortment) sits upstream and random fertilisation sits downstream, combining the meiotic products. [1 + 1]

3.3 Error 3 ("mutation only in body cells, never passes to offspring"): Mutation can occur in either body cells (somatic) or germ-line cells (eggs and sperm). Only germ-line mutations are inherited, but they absolutely do occur and are the source of new heritable alleles. Correction: relabel as "mutation in germ-line cells is heritable; mutation in body cells is not" and keep mutation as a valid source of new alleles in the population. [1 + 1]

Q4.1 — 99.6% of sibling variation (3 marks)

Crossing over during meiosis in each parent produced recombinant chromosomes carrying new combinations of P1's and P2's existing alleles [1]. Independent assortment then randomised the maternal/paternal chromosome mix in each gamete [1]. Random fertilisation finally combined a different gamete-pair to form each sibling, so each sibling carries a different reshuffle of the same parental allele pool — explaining the bulk of the differences [1].

Q4.2 — Why the G→A is a de novo mutation (2 marks)

Crossing over, independent assortment and random fertilisation can only produce new combinations of alleles already carried by the parents — they cannot generate a base that neither parent has [1]. The G→A variant is therefore not present in the parental "pool" to be reshuffled, so it must have arisen by a DNA sequence change (mutation) in a germ-line cell of one parent, since only mutation creates genuinely new alleles [1].

Q4.3 — Heritability to S2's children (1 mark)

Yes — because the variant arose in a germ-line cell of a parent and is therefore present in every cell of S2, including S2's own germ-line, it can be passed to S2's children at the normal Mendelian rate [1]. (Accept also: yes, provided the variant is in S2's germ-line cells.)