Understanding life history decisions and the reasons for phenotypic variability becomes more complicated when one considers that phenotypes do not evolve under constant environment conditions.
The old protocol has a further drawback in that phenotypes do not have a one-to-one correspondence with genotypes.
However, traits (phenotypes) do not only result from a complex combination of genetic and environmental variation but can also be influenced by epigenetic variation, which can be transgenerationally heritable in plants [10 15].
Thus, the Abl gain-of-function phenotypes do not appear to be the result of Netrin dependent repulsion.
Interestingly, these phenotypes do not usually result from Aβ1 40 expression, suggesting underlying Aβ1 42-specific neurotoxic mechAβ1 42-specific
It has been proposed that novel phenotypes do not necessarily require new genes.
These two phenotypes do not seem to be mediated by the same set of neurons.
Pathogenic phenotypes are unlikely to resemble ancestral phenotypes, and, therefore, pathogenic phenotypes do not represent reversals to the ancestral phenotypes.
Therefore, cooperative phenotypes do not necessarily have higher fitness than non-cooperative phenotypes in either poor or favorable environments.
This comprehensive inventory of cellular and molecular assays revealed that certain phenotypes correlate with HD disease CAG repeat length, whereas other phenotypes do not.
