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The striking variability in the phenotype associated with the C9ORF72 expansion suggests that multiple modifiers may exist, which may be genetic or environmental.
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For PROP and PTC, alleles of one of the 25 bitter receptors (TAS2R38) explain most of the genetic variation (5– 7) although other modifier loci may exist (8– 10).
In other words, the performance of the wax crystal modifiers may be further improved if a synergistic effect exists between EVA and solvent(s).
However, it is likely that multiple genetic modifiers for collagen IV mutations exist, and that some of these modifiers may be effective only for particular mutations (e.g. missense mutations).
Many other vehicles, pigments, and modifiers may be used.
These modifiers may be alleles of the crossveinless genes on the second and third chromosomes.
Moreover, the concerted action of several modifiers may be required to avoid disease development.
In contrast, spt-2 plants flowered significantly later than L. er, suggesting that accession specific modifiers of SPT function may exist.
9 Common genetic modifiers of some effect may exist, 90, 91 as for the congenital cardiac phenotype, 92, 93 but have not been convincingly demonstrated 67, 94– 96 (see Philip and Bassett 48 for more details), and additional copy number variation/variants (CNV) do not seem to play a major role in expression of schizophrenia.
There may exist a modifier that expresses a borderline repeat expansion.
In general, these are not equivalent because an unstable internal equilibrium may exist and the condition for successful invasion of the modifier is more restrictive than that for eventual fixation from already high frequency.
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