There is also this article from Brian:

The Genetic Factors of Silver Phenotypes
http://brianreederbreeder.blogspot.com.au/2014/02/the-genetic-factors-of-silver.html
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Originally Posted By: Redcap
So the Inhibitor of Autosomal pheomelanin (Aph^I) would be even an option to switch off (inhibit) persisting (atavistic) Autosomal red (Ar) in silver varieties?!
Quote:
By Brian Reeder: This gene inhibits the expression of autosomal pheomelanin and further helps to create the “clean white” that hobbyists desire on their silver varieties.


Who knows really, except the effects on that supposedly e+/e+ silver pullet, & others (eg e+ s+) that he has shown.

Unlike what Brian suggests in his articles, it is clear from many genetics researchers & exhibition breeders that Aph^I is not a common mutation in many clean silver domestic chicken varieties.

It's not in the exhibition Silver Duckwing MG bantam line I just purchased, it wasn't in the SL Wyandotte test bred by Moore & Smyth, not in the Silver Fayoumi, etc....
Yet Brian is saying that Aph^I is needed to produce clean silver in many silver varieties, not just Silver Duckwing (he includes Db, Co, etc based ones as well).

Quote:
When S is present instead of s+, along with Co and Db, and Aph, we see brassy silver laced with the palest area being the pheomelanin of the breast, while the rest of the pheomelanic areas are a cream to pale yellow. To secure the cleanest white in silver laced varieties, Aph^I must be present and homozygous, whether Db is present or not.


It seems he is going by phaeomelanin phenotypes only (not considering all specific mutation traits), as he also said that Db was in laced Wyandottes, that RIR were Db, not Co (some exceptions), misrepresents many of the traits of Di (no mention that it is a partial eumelanin restrictor, dilutes dermal leg pigment, etc), Mh, & so on...

So I find it very hard going reading his articles. I wish he would stick to hard data results, as he would have a wealth of information at hand from breeding these long-tails.