Axolotl

The Albino locus controls melanin synthesis via the tyrosinase enzyme. Homozygous recessive (a/a) animals completely lack the ability to synthesize melanin, eliminating all melanophore pigmentation. Xanthophores and iridophores remain functional, so an otherwise wild-type albino (D/- a/a) appears golden yellow with iridescent speckling and pink/red eyes — the "Golden Albino" phenotype. When combined with leucistic (d/d a/a), the result is the "White Albino" — a white animal with pink/red eyes and no dark pigment or freckling.

ID tips: Golden Albino (a/a with wild type D): Bright yellow/gold body with iridescent speckles. Eyes are pink to red (translucent, no melanin in iris). Gills are bright pink-red. No dark spots or freckles at any age. White Albino (d/d a/a): Pure white with pink/red eyes. No yellow coloration (xanthophores not visible against white background). Carriers (A/a) are visually indistinguishable from A/A.

The Axanthic locus controls xanthophore function. Homozygous recessive (ax/ax) animals have xanthophores that are unable to produce pteridines (yellow pigment), though the xanthophores themselves are still present and can store small amounts of dietary yellow pigments. The result is a gray to silver animal with dark melanophores and iridophores but little to no yellow coloration. Axanthic axolotls can appear similar to dark wild types, especially melanoid axanthics, making genotype confirmation from parents important.

ID tips: Axanthic (ax/ax): Gray to silver body with dark spots/speckles. No yellow or gold coloring (or very minimal dietary-derived yellow). Iridophores present (unlike melanoid), giving some iridescent sheen. Eyes are dark. Can be difficult to distinguish from some wild type individuals — lack of yellow is the key identifier. Axanthic + melanoid (ax/ax m/m) produces a very dark, nearly featureless animal that can resemble a pure melanoid.

The Copper locus controls eumelanin maturation via the Tyrp1 enzyme. Homozygous recessive (cu/cu) animals cannot fully oxidize eumelanin, producing pheomelanin (brown/red pigment) instead of eumelanin (black pigment). The result is a warm brown to copper-colored body with lighter eyes, functional xanthophores (yellow), and iridophores (iridescent). Copper axolotls are sometimes described as a form of tyrosinase-positive albinism because melanin synthesis initiates but cannot complete the full pathway to eumelanin.

ID tips: Copper (cu/cu): Warm brown to copper-tan body with lighter brown or gold-toned spots. Eyes are lighter than wild type — often amber, gold, or light brown rather than dark. Xanthophores produce visible yellow/gold tones. Iridophores present, giving iridescent highlights. Distinguished from wild type by the complete absence of black/dark brown pigment — all melanin-derived color is warm brown/copper. Distinguished from albino by the presence of melanin-derived pigment (just brown instead of black).

The Dark locus controls melanophore migration and differentiation during embryonic development. Wild type (D/-) allows normal melanophore distribution across the body. Homozygous recessive (d/d) results in the leucistic phenotype: melanophores fail to migrate from the neural crest into the skin, producing a white or pale pink animal with dark eyes. Leucistic axolotls retain the ability to synthesize melanin (unlike albinos) and commonly develop scattered dark freckles or patches on the head, gills, and dorsal crest as they mature. The d/d phenotype is the most popular and recognizable axolotl color morph in the pet trade.

ID tips: Leucistic (d/d): White to pale pink body with dark (black) eyes. External gills are pale pink from visible blood vessels. Dark freckles/spots may develop on head and gills with age. Distinguished from albino by dark eye color. Wild type carriers (D/d) are visually indistinguishable from D/D.

Green Fluorescent Protein transgene. GFP-positive axolotls express a fluorescent protein originally derived from the jellyfish Aequorea victoria. Under normal visible light, GFP axolotls appear identical to their non-GFP counterparts. Under blue or ultraviolet light, GFP-expressing tissues fluoresce bright green. The transgene segregates as a dominant trait: one copy (hemizygous/heterozygous) produces visible fluorescence. GFP can be combined with any base color morph — the fluorescence is visible in all chromatophore backgrounds, though it is most dramatic in lighter morphs (leucistic, albino) where the green glow contrasts against the pale body.

ID tips: GFP+: Under normal light, indistinguishable from non-GFP animals of the same morph. Under UV/blue light, fluoresces bright green throughout the body, with gills and eyes often showing the strongest fluorescence. Intensity varies between individuals. GFP-: No fluorescence under UV light. Confirm GFP status with a UV/blue light source — visual inspection under normal lighting is unreliable.

The Melanoid locus controls iridophore differentiation. Homozygous recessive (m/m) animals lack iridophores entirely, which eliminates the shiny/iridescent speckling seen in wild type axolotls. The absence of iridophores also triggers a secondary effect: some xanthophores convert to melanophores, resulting in increased eumelanin deposition and reduced yellow pigment. The net effect is a uniformly dark gray to jet black animal with no iridescent highlights and minimal yellow. Melanoid is one of the most visually striking axolotl morphs.

ID tips: Melanoid (m/m): Uniformly dark gray to jet black. No iridescent/shiny speckling anywhere on body (key distinguishing feature from dark wild types). Reduced yellow pigment compared to wild type. Gills are dark. Eyes are dark. Body has a matte finish rather than the slight sheen of wild types. Carriers (M/m) are visually indistinguishable from M/M wild types.