Mushroom

Crossing two of them

What it looks like on each base

It always lowers the red channel when Mu/Mu — a black horse just has almost none to lose. Whether you can see mushroom is entirely about how much pheomelanin the melanin genes left behind.

Its gene carrot

Gene key

horsegenetics.mushroom

Alleles

Mu mu

Outcomes

wild, mushroom-carrier, mushroom

Shows when

Mu/Mu only — Mu/mu is a carrier wild type

Default allele

mu

Wild frequency

1 in 34 per allele (carrier ~1 in 17)

Founder draws

1 × nextFloat()

Deterministic

yes

keep red

0.12 — cut hard, to leave the chestnut corner

red → black tint

0.34 — drops the sample down the neutral ramp

The whole gene

CoatRegions.restrictAll(ctx.skin(), f, (field, px, py, p) -> {
    float r = field.red(px, py);
    field.setRed(px, py, r * KEEP_RED);
    field.setBlack(px, py, field.black(px, py) + r * (1f - KEEP_RED) * RED_TINT_BLACK);
});

dilute() walks black sideways into red; mushroom needs the reverse, so it scales red by hand and feeds a third of what it removed back in as black. Cutting red only a little (v1 kept 0.44) barely moved a chestnut off its corner of the gradient and read as “no effect”; cutting it to ~0.12 and adding the black lands the texel near the gradient’s neutral column at a mid value — the dull grey-sepia that mushroom is.

Genetic identity

The evidence behind the variant is unusually strong for a horse colour trait. Researchers mapped mushroom to a chromosome-7 region by genome-wide association, found a shared 3 Mb homozygous region in affected ponies, and identified c.600dupC as the only high-impact candidate in it. In a phenotype-confirmed set of 96 Shetlands, all 45 mushroom ponies were Mu/Mu and none of the 51 ordinary chestnuts were (P = 1.15 × 10⁻²²). Tanaka et al., PMC6827053

Strictly, the authors wrote that the variant was proposed causal rather than proving it by gene editing. Perfect genotype-phenotype concordance, a predicted severe protein disruption, and what MFSD12 is known to do in other mammals make it a highly credible causal mutation.

Why it dilutes red and leaves black alone

MFSD12 is a membrane transporter associated with melanosomes — the pigment-making organelles inside melanocytes — and with lysosomes. Later cell biology showed that MFSD12 is required for cysteine import into melanosomes, and cysteine is needed to form cysteinyldopas, which are precursors specific to pheomelanin synthesis. Nature s41586-020-2937-x

MFSD12 activity → cysteine enters the melanosome → pheomelanin synthesis → red and yellow coat pigment

Break the transporter and the melanosomal chemistry that makes normal pheomelanin is limited, giving the muted sepia dilution. Eumelanin synthesis does not depend on that cysteine step, which is exactly why the effect is pigment-specific. Loss or altered function of MFSD12 influences pigmentation in humans, mice and dogs by the same route.

What it looks like, base by base

On a chestnut base, mushroom can look deceptively like a cream dilution, a silver-associated tone, an ordinary flaxen chestnut or just a muted chestnut. Visual identification is unreliable, and UC Davis recommends evaluating it alongside MC1R, ASIP, cream, silver, dun and the other relevant variants.

The original study found six bay Shetlands that were Mu/Mu: less red than a typical bay, black mane, tail and points retained, a more sepia body. One bay carrying mushroom and one cream allele appeared more diluted still, suggesting an additive-looking interaction on a bay background — informative, from few animals, and not a precise prediction rule.

Inheritance

Health

There is no evidence that mushroom causes systemic disease, reduced longevity, a metabolic issue, a skeletal defect or impaired athletic function. Laboratories treat it as a coat-colour test, not a disease-risk test.

The one health question actually investigated is the eye, prompted by silver’s link to multiple congenital ocular anomalies. A board-certified ophthalmologist evaluated 20 Shetlands — 9 mushroom and 11 not — while accounting for other colour genes, and found no association between mushroom homozygosity and the abnormalities observed (uveal hypopigmentation, persistent pupillary membranes, corpora nigra cysts). The ocular findings tracked tobiano and cream better in that small sample.

Worded carefully: known, no mushroom-associated eye disorder was detected in that small controlled study; not known, whether very subtle or rare ocular effects exist in a much larger population; not justified, calling mushroom proven free of any health association, since the equine evidence is limited. There is also a biological caveat — MFSD12 has melanosomal and lysosomal roles in laboratory systems, and the horse phenotype comes from a specific allele in a specific background, so human and mouse disease outcomes should not be read across.

Build, size, jumping, speed

No published evidence that the allele changes adult height or growth rate, body mass or muscling, bone structure, limb conformation, hoof quality or joint health, head and neck shape, topline, any breed-type trait, or fertility. And none that it changes maximum speed, acceleration, stride length, gait mechanics, aerobic capacity, exercise metabolism, neuromuscular power, proprioception, reaction time, balance, or jumping scope, technique, carefulness or soundness.

Breeds and frequency

In the key genotyping study the causal variant — not merely a nearby shared haplotype — was detected in only two populations among the breeds tested.

Sample estimates, not censuses: zero in 29 Icelandics does not prove the allele cannot occur in the breed. The Miniature Horse connection is historically plausible because Shetlands were a foundation breed for Miniatures and the populations have been crossed.

The mod uses one mushroom allele in 34, or 2.9% — between the Shetland 12% and the several breeds where it was not found at all, which is the right place for a world-wide founder number to sit.

What is settled, and what is not

Well supported. Mushroom is caused, or at minimum extremely strongly explained, by the recessive MFSD12 c.600dupC frameshift on ECA7; the phenotype is a dilution of pheomelanin, most visible in chestnuts as a sepia or taupe coat often with a light mane and tail; carriers show nothing; bay homozygotes show a less-red sepia body with black points retained, and black horses show little; no mushroom-specific ocular association was found in the 20-pony study; and the allele is established in Shetlands and low-frequency in Miniatures.

Plausible but unresolved. The exact magnitude and consistency of expression on bay, cream, dun and other combinations; the phenotype of a horse homozygous for both mushroom and cream, which the study had no example of; how much lighting, season, age, clipping and other colour genes change how a mushroom horse is perceived; whether rare or subtle eye findings emerge in larger studies; and whether other MFSD12 variants create mushroom-like phenotypes outside c.600dupC.

Claims to avoid. That mushroom makes horses small or pony-built; that it improves or harms jumping; that it makes a horse slower, faster, calmer or more trainable; that it is a known health defect; or that every dull chestnut, flaxen chestnut, palomino or silver-looking pony is mushroom.