Oculocutaneous albinism (OCA) is a heterogeneous genetic disorder characterized by hypopigmentation of the hair, skin, and eyes and is associated with the ocular features of nystagmus, reduced visual acuity, and misrouting of the optic fibers at the chiasm (Witkop et al., 1989). Witkop and coworkers first classified OCA into two major types, known as tyrosinase-negative OCA and tyrosinase-positive OCA, through clinical, family, and hairbulb biochemical analyses (Witkop et al., 1970, 1972, 1973). Subsequent work has identified the gene loci involved in these types of OCA and has demonstrated phenotypic variation in hy-popigmentation for each. OCA1 or tyrosinase-related OCA results from mutations of the tyrosinase gene on chromosome llq (Tomita et al., 1989; Oetting and King, 1993). OCA2 or P related OCA results from mutations of the P gene on chromosome 15q (Gardner et al., 1992; Ramsay et al., 1992; Rinchik et al., 1993; Durham-Pierre et al., 1994; Lee et al., 1994, 1995) that encodes a 110 kDa integral melanosomal membrane protein (Rosemblat et al., 1994).

OCA2 is the most common form of albinism, especially among African-Americans and Africans. It has been estimated that the frequency of OCA2 among African-Americans is 1 in 10,000. This is in contrast to a frequency of 1 in 36,000 among Caucasian-Americans (Witkop et al., 1972). The prevalence of OCA2 varies among certain African tribes and is 1 in 4,459 among the Zulu of South Africa (Kromberg and Jenkins, 1982) and 1 in 7,900 among the Bamileke of Cameroon (Aquaron, 1990). In a previous study (Durham-Pierre et al.,