Why did outcrossing rates initially rise and then fall in the evolution (static parasite) treatment?

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Question recap: Why did outcrossing rates initially rise and then fall in the evolution (static parasite) treatment?

Option a: 'Early outcrossing allowed recombination to produce resistant genotypes, which spread and eliminated the need for further genetic variation.' This is the most coherent explanation. Outcrossing increases genetic recombination, which can generate novel resistant genotypes. If those resistant genotypes spread through the population, the advantage of maintaining high outcrossing diminishes once resistance is widespread, leading to a reduction in outcrossing rates. The sequence described—rise due to beneficial recombinant resistance, followed by fall as variation becomes unnecessary—fits the expected evolutionary dynamics in a static parasite environment where host resistance is countered by recombination.

Option b: 'The parasite population became less virulent over time, so nematodes no longer needed to outcross.' This claim ties outcrossing to virulence levels, implying a direct causal link between reduced virulence and reduced need for outcrossing. However, the pattern of rising then falling outcrossing is more plausibly tied to the spread of advantageous genotypes via recombination rather than a simple decline in virulence. The statement also asserts no ongoing need for genetic exchange, which is not a well-supported general explanation for this scenario.

Option c: 'Parasite evolution in this treatment kept breaking down host resistance, favouring repeated cycles of outcrossing and selfing.' This option suggests constant host-resistance turnover prompting cycles of outcrossing and selfing. While host resistance dynamics can influence mating systems, the described pattern is a single rise and fall rather than ongoing cycling driven by continuous breakdown of resistance. It does not clearly account for the initial rise due to creation of resistant genotypes followed by a reduction once variation is no longer needed.

Option d: 'Outcrossing initially suppressed nematode reproduction, leading to population collapse and a return to selfing.' This portrays a drastic negative effect of outcrossing on reproduction, which is not typically how outcrossing dynamics work in these contexts. Outcrossing generally facilitates genetic diversity and can enhance adaptation, not cause immediate population collapse and a rebound to selfing. This makes the option biologically implausible for explaining the observed pattern.

In summary, option a provides a logically consistent sequence: outcrossing boosts recombination, produces resistance, resistant lineages spread, reducing the selective advantage of continued outcrossing, which then declines. The other options rely on assumptions about virulence, ongoing cycles, or catastrophic reproductive suppression that do not align with the described evolutionary dynamics of the static parasite treatment.

Why did outcrossing rates initially rise and then fall in the evolution (static parasite) treatment?

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