Fig. 1. (A) Reduction of ventral spot size in Kit^W/+ and Mitf^Mi-wh/+ mice with Nf1 haploinsufficiency. Nf1^+/– mice were intercrossed with Kit^W/+ mice and with Mitf^Mi-wh/Mi-wh mice. The litters at 6 weeks of age from both crosses were genotyped for Nf1. The belly-spot area in Kit^W/+ mice, wild-type and heterozygous for Nf1 and Mitf^Mi-wh/+ mice, wild-type and heterozygous for Nf1 was determined and normalized to the gram body weight of each mouse. Error bars in right panel represent standard deviation from the mean. (B) Models for the regulation of Kit-Mitf signaling by neurofibromin. Neurofibromin may regulate Kit and Mitf through their signaling axis, as depicted in the left panel, or independently through both a non-Mitf effector downstream of Kit and a non-Kit inducer upstream of Mitf. (C) Reduction of dorsal spot in Kit^W-41/+;Mitf^Mi-wh/+ mice with Nf1 haploinsufficiency. Nf1^+/–;Kit^W-41/W-41 mice were crossed with Mitf^Mi-wh/Mi-wh mice to generate Kit^W-41/+;Mitf^Mi-wh/+ compound heterozygotes Nf1^+/+ or Nf1^+/–. Mice at 6 weeks of age were genotyped for Nf1 mutational status, separated by genotype and photographed.