ZFIN is incorporating published figure images and captions as part of an ongoing project. Figures from some publications have not yet been curated, or are not available for display because of copyright restrictions.

ZFIN is incorporating published figure images and captions as part of an ongoing project. Figures from some publications have not yet been curated, or are not available for display because of copyright restrictions.

The npm Mutation Impairs Interactions between Pigment Cells

(A–D) Wild-type adult zebrafish (A), magnified mid-trunk area (B), expanded melanophores (C), and detail of 1^st ventral dark stripe in fixed specimen (D).

(E–H) npm adult mutant (E) with magnified mid-trunk area (F). The 2^nd ventral dark stripe is underdeveloped (arrow in F). Melanophores appear contracted (G). Pigmented xanthophores appear in the 1^st ventral dark stripe in fixed specimen (H; see also Figure S1).

(I and J) Number of dark stripes (I) in fish of comparable height (J) (mean ± SD, n = 10).

(K) Density of melanophores (mean ± SD, n = 10).

(L) Distance between melanophores in the 1^st ventral stripe (median ± SD, n = 10).

(M) Density of xanthophores in the first light stripe (mean ± SD, n = 10).

Pigment Pattern of npm during Development and in Double Mutants

(A) Wild-type iridophores appear as a dense sheet along the horizontal myoseptum (stages PB and PR); they spread dorsally and ventrally where they form secondary light stripes (stages J and J⁺⁺) [3].

(B) In npm mutants iridophores fail to form compact sheets. Scale bars, 250 μm.

(C) pfe mutant (top panel) compared to npm;pfeffer double mutant.

(D) shd mutant (top panel) compared to npm;shd double mutant.

npm Function Is Not Required in Pigment Cells, but in the Brain

(A) Chimeric animals (A3, A4) derived from blastomere transplantations of npm donors (A1) into nac;pfe;rse hosts (A2).

(B) Blastomere transplantations of npm;Tg(ubi:Red) donors (B1) into wild-type hosts (B2). A chimeric animal is shown (B3).

(C) Fluorescent image of an open brain (outlined).

Galanin Receptor 1A Is Mutated in npm

(A) Phenotypes of npm (A1) and CRISPR-Cas9 induced frameshift mutations in galr1A (A2), galn (A4), and a trans-heterozygous fish galr1A/npm (A3) (see also Figures S2, S3, and S4).

(B) T4 thyroid hormone levels measured in wild-type, galn, and npm mutants (mean ± SD, n = 6 for WT, n = 5 for galn, n = 4 for npm).

(C–E) Relative transcript abundance for thyroglobulin (tg; C), thyroid-stimulating hormone (tshba; D), and thyrotropin-releasing hormone (trh; E) in the heads of galn (n = 8) and npm (n = 7) mutant fish compared to wild-type (n = 9). The plots depict the mean values (horizontal line), the first and third quartiles (box), and the lowest and highest values no further than 1.5 × IQR (interquartile range) from the hinge (whiskers); outliers are plotted as individual points (^∗p < 0.09; ^∗∗p < 0.05; ^∗∗∗p < 0.01; n.s., not significant).