The molecular basis of phenotypic diversity in wild and domesticated animals is poorly understood. My project addresses how diversity arises by identifying genetic and developmental origins of unique traits. The domestic rock pigeon (Columba livia) is a compelling model to understand molecular mechanisms of diversity because this species consists of over 300 different breeds with spectacularly variable phenotypes. One derived trait, “Almond,” is characterized by seemingly random sprinkling of pigmented and apigmented regions within and between feathers throughout the body. Classical genetic studies suggest Almond feather pigmentation is caused by a dominant sex-linked mutation located near the major color locus, recently identified by our lab as Tyrp1. Additionally, these studies found that homozygous Almond males (ZZ sex chromosomes) develop severe eye defects and completely lack pigmentation whereas hemizygous Almond females (ZW), which lack a wild-type copy of the Almond allele, do not develop these defects. This suggests that dosage of the mutant allele, rather than absence of the wild-type allele, is responsible for these eye phenotypes. We compared the genomes of 10 Almond pigeons to 76 non-almond pigeons of various colors using pFst in order to identify a candidate region on scaffold 6 a Z chromosome scaffold. Further investigation showed a substantial increase in coverage in this region in Almond birds, indicative of copy number variation in this region. There are 5 genes in this region including MLANA, a melanosome maturation gene. Expression analysis using Q-RT-PCR on regenerating feathers revealed a suprising decrease in MLANA expression in the light feathers of Almond birds despite a increase in copy number. Currently no coding changes have been found in the genes in this region, indicating that substantial increase in copy number of MLANA leads to the sprinkling feathers and eye defects seen in Almond pigeons.