eye assay. This simple assay uses the hypopigmented golden mutant, the very first mutant studied in zebrafish genetics. This simple assay uses gol=þ heterozygotes to detect somatic mutations as pale retinal-pigmented epithelial cells (gol=gol*) in a background of black (gol=þ) cells. Finding gin mutants and their cancer susceptibility left us with the need to identify the golden gene. That in turn led me to ask why the golden mutant is lighter in color than wild-type zebrafish. An ultra- structural comparison revealed something startling: lighter skin in both golden zebrafish and Europeans show a decrease in number, size, and pigment density of melanosomes. The golden gene turned out to be a new pigmentation gene,slc24a5, or nckx5, governing sodium-calcium exchange. Analysis of the online database of human genetic variation, the HapMap, together with studies of human populations of mixed ances- try, allowed us to conclude that the human ortholog had undergone an adaptive mutation during the evolution of the light skin color in Europeans. But that's just the first half of the human pigmentation story—we still need to know what is responsible for the light skin of East Asians=Amerindians! The huge social consequences of the ''scientific'' connections drawn between skin color and ''race,'' together with the po- tential to contribute to society's understanding of skin color and our common ancestry, have now drawn me profession- ally into an entirely new field. Stephen C. Ekker: Between the two of you, then, we have what might be called the two ends of the spectrum of zebra- fish pigment biology. And that realm of zebrafish study, numbering many investigations, dates far back into the his- tory of the field. Can you each name some of the papers that have been the most influential in affecting the way you look at zebrafish pigment biology?