Natural gene / eyes only
Tiger eye (SLC24A5)
A bright amber iris in a horse whose coat is entirely ordinary. It is the first gene in the mod that changes only the eyes, and the reason the eye-colour channel exists at all. Essentially confined to the Puerto Rican Paso Fino, in life and here.
Crossing two of them
Where to find it
SLC24A5 is a Puerto Rican Paso Fino gene,
essentially confined to that breed in life, and it is distributed that way here: a
quarter of Paso Finos carry a copy and about one in twenty-five has the amber eyes,
against roughly one wild horse in five thousand. It is the clearest case in the mod of
a gene you find by knowing which breed to look in — and since the breed is
RARE and spawns in jungle, savanna, beach and mangrove swamp, finding one
is a trip rather than a wait.
Its gene carrot
- Gene key
- horsegenetics.tiger_eye
- Priority
- 60 (natural band, after grey, before the white loci)
- Alleles
- TE1 TE2 N
- Combinations
- 6, all carryable — 4 outcomes
- Outcomes
- wild,
tiger-eye-carrier(a wild type),tiger-eye-amber,tiger-eye-yellow - Default allele
- N
- Wild frequency
- ~1 in 70 per
TE1, rarer forTE2— but 26% of Puerto Rican Paso Finos carry a copy - Founder draws
- 1 × nextFloat()
- Coat effect
- the iris texels only — deterministic, so it is out of the per-horse texture fingerprint
The iris colour is asserted through the real pipeline in
EyeColorTest — a bay's black iris comes out
#C8811E and its sclera stays white. What is unknown is whether a
two-texel gold iris reads as a gold eye on a horse at riding distance,
or whether it needs to be brighter. Checklist on
To be verified.
The combination table
| Combination | Outcome | Effect |
|---|---|---|
N/N | wild | Ordinary dark eyes |
TE1/N, TE2/N | tiger-eye-carrier | Nothing at all — not in the eyes, not in the coat |
TE1/TE1, TE1/TE2 | tiger-eye-amber | Asks the iris loci for Gld |
TE2/TE2 | tiger-eye-yellow | The same request. See the note below — the paler shade is gone. |
Recessive: one wild-type copy and nothing shows, so two carriers bred together is the only way amber eyes appear. The two variants are the same trait a stop apart in shade — which is what a combination table is for, and cheaper than inventing two genes.
It is not a coat pattern
Worth saying, because the breed reference this mod was built from files tiger eye under coat patterns and it is not one. The coat is completely unaffected; only the iris changes. That is precisely why it could not be built until the eye-colour channel existed — there was nowhere for it to write.
It does still affect the baked coat texture, because the eyes are
drawn into it. So unlike the mod's other "paints nothing" genes, its expressing
outcomes are real markers rather than wild types: they stay in
Genotype.coatCode(), and two horses that differ only here do not share a
cached texture. They are deterministic — every gold eye is the
same gold — so the cache pays one entry per outcome and not one per horse. What is
actually in the key now is the iris locus the request wrote
to, which comes to the same thing.
The eye-colour channel
A horse has one iris colour, so "what colour are its eyes" has exactly one answer and several genes have a claim on it. That makes it a channel with a single owner and a contribution hook, like the LUT and the cutie mark — not a gene that other genes fight with. Tiger eye is why it exists: it was the first gene in the mod with nowhere else to write.
The channel is now the whole account of a horse's eyes — the three ranks, the dilutions' green and hazel, the white loci's blue, complete and sectoral heterochromia, and how a gene joins in — and it lives on Eye colour & heterochromia. Only what is about this gene is repeated here.
Tiger eye does not paint an iris. It asks for one. It implements
EyeRequestContribution and requests EyeHue.GOLD at both iris
loci; Eyes.force writes the allele onto the horse when the horse is made.
So a tiger-eye horse is genuinely Gld/Gld at both eyes — it shows the
gold, and it passes the gold on, tiger eye or no tiger eye.
The old rank argument survives as ordinary gene order. Tiger eye sorts before the four white loci and after the dilutions, and requests merge last-writer-wins — so a cremello that also carries tiger eye has gold eyes, and a splashed white tiger-eye horse has blue ones, for exactly the reasons they always did and without a rank number to maintain. See when two genes both ask.
TE1’s amber and TE2’s paler yellow were two
hex values this gene owned. The colour vocabulary is closed now —
EyeHue is a fixed list of alleles, because a hue no allele can name is a
hue nobody can breed toward — and both shades map to Gld. The
two outcomes are still separate combinations and still separately breedable, but they
look the same. If the pale form is worth keeping it wants an allele at the
iris locus, not a constant here.
A white locus’s request frequently fails to reach both irises, and the eye it does not reach was never asked about — so it keeps tiger eye’s gold. A splashed white tiger-eye horse may well come out with one blue eye and one gold one, or with a blue wedge in a gold iris, and unlike before both of those are alleles it carries. See the spread.
The gene
| Gene | SLC24A5 — solute carrier family 24 member 5 |
|---|---|
| Protein | A potassium-dependent sodium/calcium exchanger, thought to work in the trans-Golgi network of melanocytes and to take part in melanosome maturation |
| Chromosome | Equine chromosome 1 (ECA1). The mapping interval was roughly 3.5 Mb; in EquCab2 coordinates the gene sits at about chr1:141,657,837–141,678,329 |
| Inheritance | Simple autosomal recessive |
| Phenotype | A dilute iris — bright yellow, amber or orange. No known coat effect |
| Breed | Puerto Rican Paso Fino |
Across vertebrates, SLC24A5 is a major pigmentation gene. Disrupting it in zebrafish gives the well-known “golden” phenotype; common variation in humans contributes to skin-pigmentation differences, and some biallelic damaging variants cause oculocutaneous albinism type 6. The most relevant cousin is the mouse: loss-of-function work there implicates it particularly in the pigmentation of ocular tissues — iris and retinal pigment epithelium — while the body coat stays fairly normal. That is precisely the pattern the horse shows, which is a large part of why the candidate was convincing. Mack et al., PMC5555483
Cross-species evidence makes the gene compelling; it does not license assigning effects seen in people, mice or fish to a tiger-eyed horse.
Two alleles, one of them barely characterised
| allele | molecular change | protein consequence | status |
|---|---|---|---|
| TE1 | exon-2 missense, c.271A>T in the study transcript (modern annotation c.272A>T) | p.Phe91Tyr — a highly conserved phenylalanine becomes tyrosine near the first predicted transmembrane / cation-exchange region | predicted damaging; the best-supported and commonest allele |
| TE2 | a 628-bp deletion, c.875-340_1081+82del, removing all of exon 7 plus adjacent intronic sequence | in-frame loss of 69 amino acids (residues 292–360), removing part of the connecting loop and two transmembrane helices | structurally persuasive; much more sparsely characterised |
Phe91 was conserved across the 100 vertebrates examined, and TE1 was computationally predicted deleterious. TE2 is persuasive because it deletes an entire exon and parts of the predicted ion-exchange membrane architecture. Both rest on association and genotype-phenotype evidence rather than direct functional experiments in horse melanocytes.
The iris, which is the whole of the established effect
A dilute iris — bright yellow, amber or orange, called tiger-eye or goat-eye. It occurs in either sex and has been seen on black, bay and chestnut bases.
What makes it unusual is the company it does not keep. Cream changes coat and eye; double cream dilutes commonly have blue eyes. Champagne dilutes the coat and goes with amber eyes. Several white-spotting patterns associate with blue eyes. Tiger eye is the first well-characterised equine iris-pigmentation locus reported with no accompanying coat dilution or white-pattern effect at all.
This page and the source agree emphatically: the coat is unaffected and only the iris
changes. That is why the gene needed
the eye-colour channel to exist before it could
be built at all — there was no way to express “changes the horse, paints
nothing” until EyeColorContribution did.
For TE1 homozygotes and TE1/TE2 compound heterozygotes the study found no apparent coat-colour change: tiger-eye animals occurred across all three non-dilute bases, there was no association between chestnut status and stronger yellow or orange expression, and no visible relationship between iris shade and coat colour.
The TE2 homozygote, and what the mod asserts about it
There is one documented TE2/TE2 horse. It was a palomino with
blue / light yellow-blue eyes — and because it also carried one cream allele, the
researchers could not separate a possible TE2 effect from cream’s known eye-pigment
effect, or from an interaction between the two.
So “TE1 has no obvious coat effect” is reasonably supported, and
“TE2/TE2 never affects coat or eye beyond tiger-eye” is not
established. It is speculative but biologically plausible that a severe TE2-related
reduction of SLC24A5 function produces a stronger ocular phenotype in some
backgrounds.
TE2/TE2 a definite colour the literature does not have
TigerEyeGene resolves TE2/TE2 to a distinct paler,
greener-yellow iris — tiger-eye-yellow, a separate outcome from the
amber that TE1/TE1 and TE1/TE2 give. That is an extrapolation
from a single horse whose phenotype was explicitly confounded by cream, and it
is the one place this locus states something firmer than its source.
It is a defensible extrapolation — a more disruptive allele giving a more diluted
iris is exactly what the mechanism predicts — and a game cannot render
“unresolved”. But if the mod ever wanted to be conservative here, collapsing
TE2/TE2 into the same amber as the other two would cost one catalogue entry
and would match what anyone has actually observed.
Inheritance
| genotype | expected iris | breeding |
|---|---|---|
N/N | usual dark brown or black | cannot pass either variant |
N/TE1, N/TE2 | usually brown-eyed — a phenotypically normal carrier | 50% chance of passing it per foal |
TE1/TE1 | tiger eye | passes TE1 to every foal |
TE1/TE2 | tiger eye — a compound heterozygote | passes TE1 or TE2 to every foal |
TE2/TE2 | expected light iris; very rare in the documentation | passes TE2 to every foal |
Not sex-linked. Two carriers give the classic 25% affected, 50% carrier, 25% clear. The
principle that matters with two alleles is that any pair of tiger-eye alleles
combines — TE1/TE2 is affected exactly as TE1/TE1 is,
which is why a carrier of one variant and a carrier of the other can produce a tiger-eyed
foal between them. The mod implements this directly: expressionOf asks only
whether a wild-type copy is present.
The original pedigrees fit recessive inheritance well: tiger-eye × tiger-eye matings produced five tiger-eyed offspring in the available data, and brown-eyed parents occasionally produced tiger-eyed foals — consistent with unrecognised carriers.
Health and vision
Reassuring, and thin. A board-certified veterinary ophthalmologist examined three
tiger-eyed Puerto Rican Paso Finos — two TE1/TE1, one
TE1/TE2 — against three dark-eyed controls. Beyond iris pigment the study
reported no ocular abnormalities attributable to tiger eye, no visual deficits, no reduction
of pigment in the retina or retinal pigment epithelium, and none of the human-OCA-like signs
a more severe pigment disorder would predict — no obvious photophobia, nystagmus or
reduced acuity. One tiger-eyed horse had an eyelid-margin defect and a limbal dermoid, which
the authors considered unrelated.
“Not observed” is not “proven absent.” The formal ophthalmic
sample was six horses in total; the single known TE2/TE2 horse was not
given a specialist exam; no large or long-term surveillance has tested light sensitivity,
retinal physiology, visual behaviour or subtle visual performance; and there is no direct
evidence that tiger eye either causes or prevents eye disease.
The defensible statement: TE1/TE1 and TE1/TE2 have not been
shown to impair vision or create a health disorder, and rare effects and the
TE2/TE2 phenotype remain under-studied. The mod carries no health cost at
this locus, which matches.
Build, size, speed, jumping
| trait | evidence for a TE1 or TE2 effect |
|---|---|
| height or mature size | none |
| bone, body mass, muscling, build | none |
| conformation | none |
| gait mechanics, Paso Fino gait quality | none |
| aerobic capacity, endurance | none |
| sprint speed, racing performance | none |
| jumping scope, technique, soundness | none |
| temperament, trainability | none |
The original work was a pigmentation study — eye photographs, pedigrees, sex and coat-colour observations, then genetic mapping. It phenotyped no height, conformation, locomotor biomechanics, race times, jumping results, muscle traits, metabolic variables or veterinary outcomes beyond the small ophthalmic assessment. It therefore cannot support a performance claim in either direction.
See a gene expressed in several tissues, or a pigment gene with health effects in another species, and infer that it changes horse athleticism. The mapped signal here is for iris pigmentation, and sitting on chromosome 1 does not make it a speed locus. Claims that tiger-eyed horses are faster, lighter-built, better jumpers or weaker athletes are breeder lore until someone produces a controlled study with genotype-confirmed horses and objective measurements.
Breed and frequency
TE1 and TE2 are documented in the Puerto Rican Paso Fino, and in no other breed. The distinction matters, because “Paso Fino” covers related but genetically distinct populations — the evidence concerns Puerto Rican Paso Finos specifically, not every horse registered broadly as a Paso Fino.
The original study screened 196 horses from related Iberian-origin populations:
| breed | n | TE1 or TE2 detected? |
|---|---|---|
| Colombian Paso | 90 | no |
| Lusitano | 44 | no |
| Andalusian | 42 | no |
| Mangalarga | 20 | no |
| total | 196 | no alleles found |
All were homozygous reference at both sites. Strong evidence of absence from that sample; not proof of absence from every animal, bloodline or cross in those breeds.
A breed-wide allele frequency is not established. The dataset was assembled
around phenotype discovery rather than as a random registry survey, so its raw counts are not
a prevalence estimate. What can be said: of 216 Puerto Rican Paso Finos photographed, 32 were
classified tiger-eyed after exclusions — about 14.8% of the photographed group,
and explicitly not a reliable prevalence figure, since the sampling was not random
and many horses were excluded for intermediate, blue or dilution-associated phenotypes. Of
those 32, 20 were TE1/TE1 and 8 were TE1/TE2, so the two
alleles explained 28 of 32 cases — 88%.
The four unexplained cases are instructive. Three were heterozygous TE1 carriers with orange eyes at the darker end of the study’s range, and may simply have been borderline light-brown. One was a yellow-eyed TE1 carrier that could plausibly carry an undiscovered second SLC24A5 allele — but the horse was dead and could not be rechecked.
The conclusion: TE1 is probably the predominant documented allele, TE2 is rarer, and exact frequencies await a modern random breed survey. The mod encodes that ordering — TE2 is set at 0.6× TE1’s frequency — which is the right shape from a 20-against-8 split, and the absolute figure of one allele in 70 wild horses has no published counterpart to check against. What the mod does have, and what this page supports, is the concentration: this is the clearest case in the mod of a gene you find by knowing which breed to look in.
What is settled, and what is not
Established. Tiger eye is a recessive iris-colour trait in Puerto Rican Paso
Finos; the locus is on ECA1 and involves SLC24A5; TE1/TE1 and
TE1/TE2 commonly produce yellow, amber or orange irides; the two alleles explain
most but not every classified case; neither was found in the 196 related-breed horses tested;
neither has a demonstrated coat effect; and in a very small specialist sample they were not
associated with any detected ocular or visual deficit.
Plausible but unproven. That the variants dilute iris pigment by altering ion
handling and melanosome maturation. Whether the amber result reflects reduced eumelanin, an
altered eumelanin-to-pheomelanin balance, altered pigment quantity, altered melanosome
packaging or some combination — none of which has been measured in tiger-eyed horse
iris tissue. That TE2/TE2 gives a more extreme phenotype and might interact with
cream, which one confounded horse cannot settle. That further undiscovered
SLC24A5 variants, or variants elsewhere, explain the phenotype-genotype mismatches.
And that the alleles might exist at very low frequency in unsampled related breeds.
Unsupported. That tiger eye changes coat colour in ordinary
TE1/TE1 or TE1/TE2 horses; that it changes height, body type,
strength, gait, speed, jumping, endurance or trainability; that it is itself a disease or
causes blindness; or that every amber, hazel, yellow or blue eye in a horse comes from
SLC24A5 — iris colour also arises from cream, champagne, white spotting and
other contexts, and phenotype alone is not a test. The mod encodes that last point
structurally: tiger eye contributes its colour at
RANK_PIGMENT, so a tiger-eye horse that is
also splashed white has blue eyes rather than amber — there is no pigment left
in a depigmented iris for this gene to colour.