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The heterozygous plants were intermediate between the homozygotes in both traits.
For example, serotonin and dopamine pathways have been found to be involved in both traits and may be involved in both traits independently.[5], [6] Alternatively, low intelligence and neuroticism may share causal determinants as they are closely related to symptoms of depression and socioeconomic status.
This lack of correlation can be explained by putative constraints in the evolution in both traits, such as the minimum genome size or the proportional evolution for GS, and the lower responses of FD to selection in self-compatible species, as already discussed.
If anything, a trend towards greater lamination is found in type 1 brains, instead of in type 2. It must be considered also that those species that present significant evolutionary changes in both traits are also those that present the higher degree of lamination and cell specialization in their groups.
One model that could explain the observed responses in both traits is differential epistasis [ 62].
Thus the QTL have resulted in a reduction in polygenic variance of 42% in both traits.
Significant decreases in both traits have been reported during advanced cycle breeding [ 13].
This number would have been too small to examine the interaction between the pathways involved in both traits.
Variation in both traits has severe effects on fitness: age at maturity affects generation time and size at maturity has a strong effect on reproductive capacity.
Moreover, we assumed that infectivity and susceptibility are independent, which is the case where the model benefits most from accounting for variation in both traits.
In this sense, only around one third of the QTL epistatic interactions detected in the current study were coincident in both traits.
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