Natural gene / phase 1
Silver dapple
Real-horse PMEL17. Silver dilutes eumelanin only —
it walks black toward chocolate, and the mane and tail most of the way to flaxen,
while leaving red pigment completely alone. A chestnut that carries it looks
identical to one that doesn’t: it has no black for silver to act on.
Crossing two of them
What it looks like on each base
| Base | Name | Result |
|---|---|---|
black (E_ aa) | silver / chocolate | chocolate body, flaxen mane & tail |
bay (E_ A_) | silver bay | red body untouched, points diluted to chocolate, flaxen mane / tail |
chestnut (ee) | — | no visible change (carrier) |
Its gene carrot
- Gene key
- horsegenetics.silver
- Alleles
- Z z
- Outcomes
- wild,
silver - Shows when
Z/z,Z/Z- Default allele
- z
- Wild frequency
- 1 in 60 per allele
- Founder draws
- 1 × nextFloat()
- Deterministic
- yes
- body
- keepRed 0.90, keepBlack 0.46, tint 0.30 — chocolate
- mane / tail / ears
- keepRed 0.40, keepBlack 0.10, tint 0.28 — flaxen
The whole gene
boolean hair = part == Part.MANE || part == Part.TAIL
|| part == Part.LEFT_EAR || part == Part.RIGHT_EAR;
f.dilute(px, py,
hair ? HAIR_KEEP_RED : BODY_KEEP_RED, // body barely touches red;
hair ? HAIR_KEEP_BLACK : BODY_KEEP_BLACK, // the mane pulls red down too, so it
hair ? HAIR_BLACK_TINT : BODY_BLACK_TINT); // leaves the dark-red corner - flaxen
On the body silver keeps almost all the red and just cuts the black, so a black horse’s eumelanin walks to a warm chocolate. The mane, tail and ears pull the red down as well, so the sample leaves the dark-red corner of the gradient and comes out flaxen rather than chestnut — the light mane on a dark body that names the gene. (v1 kept red at 1.0 on the mane and it came out a reddish chestnut instead.)
MCOA — the eye defect that rides along
A homozygous silver carries multiple congenital ocular anomalies: cysts and a malformed cornea, and a horse that sees badly. The mod has no vision for a horse to lose, so it is priced the way every sub-lethal disorder here is priced — two hearts. It shows in the info panel and the paper dump by name.
| combination | coat | health |
|---|---|---|
Z/Z | silver dapple | MCOA — −2 max health |
Z/z | silver dapple | nothing — sound eyes |
z/z | wild type | nothing |
Only the homozygote. A single copy gives the whole coat with none of the defect, which is exactly why the disorder survives in a real population: the gene people breed for is the gene that hides it. Machinery on the horse’s body.
Why it runs after agouti
Silver only has something to do once the black points exist, so in
Genes.naturalOrder() it sits immediately
after agouti: agouti paints the mane / tail / leg
black, silver then lightens it. Put the other way round and a bay’s mane
would be re-blackened after silver had already flaxened it.
- The dappling that gives the gene its name is not built — v1
is the dilution only. A deterministic dapple field (a fixed-seed
BodyNoisemodulation, like grey’s but lighter and per-genotype rather than per-horse) is the obvious next step. - The flaxen mane still reads a little gold rather than pale.
- Health:
Z/Z→ MCOA (multiple congenital ocular anomalies) is built — an impairingConditioncosting two hearts. See the horse’s body.
common/genetics/genes/SilverGene.java