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    1. In the index patient (IV1) of family OA1-3 that did not show exon deletion, sequence analysis of all coding exons including the exon-intron boundaries revealed a deletion of a single nucleotide G at position 310 of the cDNA introducing a subsequent premature stop codon one codon downstream, predicting a deleterious protein product. This newly described mutation (310delG) in exon 2 of the OA1 gene creates a TaqI restriction site. Although the pedigree of family OAI-3 initially suggested the patient IV1 to be a sporadic case, PCR-restriction analysis identified the patient's maternal uncle (III3), known to have only a decreased visual acuity at age 38, as hemizygous for the mutation. The mother (III2) and the maternal grand-mother (II1) of the proband were found to be carriers (Fig. ​(Fig.4B),4B), as expected

      Case#: Faugere_2003_Family_OA1-3_Patient_IV1, male, 26 years of age at time of report, family origin reported to be from the South of France with race described as Caucasian

      CasePresentingHPOs: HP:0006934 (Congenital nystagmus), HP:0007750 (Hypoplasia of the fovea), HP:0007663 (Reduced visual acuity), HP:0001089 (Iris atrophy), HP:0012805 (Iris transillumination defect), HP:0007894 (Hypopigmentation of the fundus), HP:0030602 (Abnormal fundus autofluorescence imaging), HP:0030479 (Abnormal amplitude of light-adapted flicker electroretinogram)

      CaseHPOFreeText: The proband was initially diagnosed with congenital nystagmus.

      CaseNotHPOs: HP:0012632 (Abnormal intraocular pressure), HP:0000518 (Cataract)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing was not described, however, the proband was examined for whole-exon deletions using PCR amplification of the 9 exons from the GPR143 locus.

      CaseMethod1: Sanger sequencing

      CaseMethod2: Restriction enzyme analysis using TaqI

      CaseGenotypingMethod: The proband was examined for whole-exon deletions using PCR amplification of the 9 exons from the GPR143 locus, followed by Sanger-based sequencing and restriction enzyme-based screening of family members using TaqI.

      Variant: The proband harbors the NM_000273.3(GPR143):c.310del (p.Asp104fs) variant in the hemizygous state.

      ClinVar: 98625

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.310del (p.Asp104fs) is a frameshift variant in exon 2 of 9, and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 75% of the protein product.

      CaseAddInfo: While the proband was initially thought to be a sporadic case, the variant was later found to be maternally inherited, with an uncle found to harbor the variant and to be affected with decreased visual acuity. Further details of the family member are not described.

      CasePMIDs: N/A

    1. Novel GPR143 mutations and clinical characteristics in six Chinese families with X-linked ocular albinism

      PMID: 18978956

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    2. c.849delT (p.Val284SerfsX15)

      Case#: Fang_2008_Family_1_Patient_IV16, male, age 8 at time of report, family national origin reported to be from China

      CasePresentingHPOs: HP:0000639 (Nystagmus), HP:0030534 (Abnormal best corrected visual acuity test), HP:0007750 (Hypoplasia of the fovea)

      CaseHPOFreeText: The proband and his affected family members have been diagnosed with ocular albinism 1.

      CaseNotHPOs: HP:0007730 (Iris hypopigmentation), HP:0007894 (Hypopigmentation of the fundus)

      CaseNotHPOFreeText: albinotic fundus

      CasePreviousTesting: N/A

      CaseMethod1: Sanger sequencing

      CaseMethod2: N/A

      CaseGenotypingMethod: The proband was genotyped by Sanger sequencing of PCR products from the 9 exons of the GPR143 gene.

      Variant: The proband harbors the NM_000273.3(GPR143):c.849del (p.Val284SerfsTer15) variant in the hemizygous state.

      CAID: CA2573320706

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.849del (p.Val284SerfsTer15) is a frameshift variant in exon 7 of 9, predicted to trigger nonsense-mediated decay or to at least truncate 30% of the protein product.

      CaseAddInfo: The family of the proband includes at least 7 other affected males and 4 unaffected female carriers.

      CasePMIDs: N/A

    1. Identification of a novel GPR143 mutation in a large Chinese family with congenital nystagmus as the most prominent and consistent manifestation

      PMID: 17516023

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    2. p.S89F

      Case#: Liu_2007_Family_Patient_V-10, male, age <6 months at time of onset, family origin reported to be Chinese

      CasePresentingHPOs: HP:0006934 (Congenital nystagmus), HP:0000666 (Horizontal nystagmus), HP:0007750 (Hypoplasia of the fovea), HP:0000483 (Astigmatism), HP:0007663 (Reduced visual acuity), HP:0007814 (Retinal pigment epithelial mottling), HP:0000646 (Amblyopia)

      CaseHPOFreeText: The proband and his affected family members have been diagnosed with congenital nystagmus segregating with an X-linked mode of inheritance.

      CaseNotHPOs: HP:0001000 (Abnormality of skin pigmentation), HP:0009887 (Abnormality of hair pigmentation), HP:0012805 (Iris transillumination defect), HP:0007894 (Hypopigmentation of the fundus), HP:0000545 (Myopia)

      CaseNotHPOFreeText: The patient did not exhibit abnormalities of the optic nerve head on functional MRI.

      CasePreviousTesting: Linkage mapping has been performed in affected and unaffected family members using 33 polymorphic markers along the entire X chromosome. Haplotype analysis identified a shared region of approximately 10.6 Mb in all affected males.

      CaseMethod1: Linkage mapping and haplotype analysis

      CaseMethod2: Sanger sequencing of 21 candidate genes in the linkage region

      CaseGenotypingMethod: Linkage mapping has been performed in the proband and affected and unaffected family members using 33 polymorphic markers along the entire X chromosome. Haplotype analysis identified a shared region of approximately 10.6 Mb in all affected males. Sanger sequencing was then performed for 21 candidate genes in the linkage region, followed by RFLP analysis in a subset of affected and unaffected family members.

      Variant: The proband harbors the NM_000273.3(GPR143):c.266C>T (p.Ser89Phe) variant in the hemizygous state.

      ClinVar: 10522

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.266C>T (p.Ser89Phe) is a missense variant in exon 2 of 9 total, and is located in a transmembrane domain but does not have experimental evidence of gene impact.

      CaseAddInfo: The proband is from a family with at least four other affected males and one affected female family member who also harbor the variant.

      CasePMIDs: N/A

    1. Morpholino-mediated knockdown of OA1 (also known as GPR143), mutations in the human homologue of which cause the most common form of human ocular albinism, induces a major reduction in melanosome number, recapitulating a key feature of the mammalian disease where reduced melanosome numbers precede macromelanosome formation.

      ExperimentName: Zebrafish knockdown of the GPR143 ortholog OA1

      NonHumanModel: Danio rerio

      GeneAlteration: A zebrafish model of OA1 loss-of-function was generated by morpholino-based knockdown.

      ModelPhenotype: HP:0007703 (Abnormality of retinal pigmentation)

      HumanPhenotype: HP:0000639 (Nystagmus), HP:0003593 (Infantile onset), HP:0007663 (Reduced visual acuity), HP:0001361 (Nystagmus-induced head nodding), HP:0000646 (Amblyopia), HP:0000483 (Astigmatism), HP:0000613 (Photophobia), normally pigmented skin and hair, HP:0005592 (Giant melanosomes in melanocytes), HP:0007750 (Hypoplasia of the fovea), HP:0007894 (Hypopigmentation of the fundus), HP:0025551 (Optic nerve misrouting)

      ModelEvidence: The zebrafish match one feature of the human patients in that they exhibit abnormalities of retinal pigmentation consistent with the ability of GPR143 loss-of-function to trigger defects in melanosome regulation (Figure 1).

      ModelVariant: This model features disruption of OA1 expression by knockdown, and does not harbor a mutation equivalent to a variant from a human patient.

    2. Regulation of melanosome number, shape and movement in the zebrafish retinal pigment epithelium by OA1 and PMEL

      PMID: 25690007

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    1. P6 (father of P1, P2, P3) was hemizygous for the mutation c.461del_T (p.Ile154fs) in GPR143/OA1 and is described in the Supplement.

      Case#: Paavo_2018_Patient_6, male, 43.1 years of age at time of report, family origin reported as Hispanic

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The proband has been diagnosed with ocular albinism 1.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: It is not clear whether previous genotyping was performed.

      CaseMethod1: Sanger sequencing

      CaseMethod2: N/A

      CaseGenotypingMethod: The patient's family appears to have been genotyped by Sanger sequencing of the 9 exons from the GPR143 gene.

      Variant: The proband harbors the NM_000273.3(GPR143):c.461del (p.Ile154fs) variant in the hemizygous state.

      ClinVar: 817370

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.461del (p.Ile154fs) is a frameshift variant in exon 4 of 9, and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 62% of the protein product.

      CaseAddInfo: The proband has three daughters who carry the variant in the heterozygous state but are reportedly unaffected, other than one daughter reporting difficulty seeing in the dark.

      CasePMIDs: N/A

    1. Clinical features of affected males with X linked ocular albinism

      PMID: 8494858

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    1. c.333_360+14del42insCTT

      Case#: Zou_2017_Patient_F1-II:1, male, age 4 at time of report, family national origin reported to be from China

      CasePresentingHPOs: HP:0000639 (Nystagmus), HP:0000613 (Photophobia), HP:0007663 (Reduced visual acuity), HP:0007750 (Hypoplasia of the fovea), HP:0007894 (Hypopigmentation of the fundus)

      CaseHPOFreeText: The proband has been diagnosed with ocular albinism 1. Foveal hypoplasia was described as severe. Best-corrected visual acuity was limited to light perception.

      CaseNotHPOs: HP:0007730 (Iris hypopigmentation)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      CaseMethod1: Sanger sequencing

      CaseMethod2: N/A

      CaseGenotypingMethod: Patients were genotyped by Sanger sequencing of PCR products from the 9 exons of the GPR143 gene.

      Variant: The proband harbors the NM_000273.3(GPR143):c.333_360+14delinsCTT variant in the hemizygous state.

      CAID: CA2573320702

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.333_360+14delinsCTT is an indel variant removing the 3' end of exon 2 including the canonical splice donor site, and is predicted to either introduce a premature stop codon or exon skipping.

      CaseAddInfo: N/A

      CasePMIDs: N/A

    2. c.793C>T (p.R265X)

      Case#: Zou_2017_Patient_F3-III:3, male, age 24 at time of report, family national origin reported to be from China

      CasePresentingHPOs: HP:0000639 (Nystagmus), HP:0000613 (Photophobia), HP:0007663 (Reduced visual acuity), HP:0007750 (Hypoplasia of the fovea), HP:0007894 (Hypopigmentation of the fundus), HP:0007730 (Iris hypopigmentation), HP:0030534 (Abnormal best corrected visual acuity test)

      CaseHPOFreeText: The proband has been diagnosed with ocular albinism 1. Foveal hypoplasia was described as severe. Best-corrected visual acuity was limited to light perception.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      CaseMethod1: Sanger sequencing

      CaseMethod2: N/A

      CaseGenotypingMethod: Patients were genotyped by Sanger sequencing of PCR products from the 9 exons of the GPR143 gene.

      Variant: The proband harbors the NM_000273.3(GPR143):c.733C>T (p.Arg245Ter) variant in the hemizygous state.

      ClinVar: 1352731

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.733C>T (p.Arg245Ter) is a nonsense variant in exon 6 of 9, and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 40% of the protein product.

      CaseAddInfo: N/A

      CasePMIDs: N/A

    1. Localization of the X-linked ocular albinism gene (OA1) between DXS278/DXS237 and DXS143/DXS16 by linkage analysis

      PMID: 2280973

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    1. Identification of a novel GPR143 deletion in a Chinese family with X-linked congenital nystagmus

      PMID: 18523664

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    2. In this study, we collected data from a four-generation Chinese family with X-linked congenital nystagmus. All the affected individuals suffer from nystagmus and amblyopia but without any sign of retinal hypopigmentation. We mapped the disease-causing gene to Xp22.3 and found a 37-bp deletion in exon 1 of GPR143 in all affected male and female carriers.

      Case#: Zhou_2008_Patient_III:22, male, age of onset not reported, family origin reported to be from China

      CasePresentingHPOs: HP:0000639 (Nystagmus), HP:0000646 (Amblyopia)

      CaseHPOFreeText: The proband has been diagnosed with congenital nystagmus.

      CaseNotHPOs: HP:0040030 (Chorioretinal hypopigmentation)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Genotyping was initially performed by linkage mapping using 26 short tandem repeat markers on the X chromosome.

      CaseMethod1: linkage analysis

      CaseMethod2: Sanger sequencing

      CaseGenotypingMethod: Genotyping was initially performed by linkage mapping using 26 short tandem repeat markers on the X chromosome, followed by Sanger sequencing of PCR products from each exon of the GPR143 gene.

      Variant: The proband harbors the NM_000273.3(GPR143):c.162_198del (p.Ala55fs) variant in the hemizygous state.

      ClinVar: 10524

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.162_198del (p.Ala55fs) is a frameshift variant in exon 1, and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 87% of the protein product.

      CaseAddInfo: The proband is from a family with at least seven other affected males who also harbor the variant.

      CasePMIDs: N/A

    1. We provide here structural evidence that the protein product of the ocular albinism type 1 gene (OA1), a pigment cell-specific integral membrane glycoprotein, represents a novel member of the GPCR superfamily and demonstrate that it binds heterotrimeric G proteins. Moreover, we show that OA1 is not found at the plasma membrane, being instead targeted to specialized intracellular organelles, the melanosomes. Our data suggest that OA1 represents the first example of an exclusively intracellular GPCR

      Selection B- Gene function is consistent with phenotype.

      Title: GPR143 binds heterotrimeric G proteins and shows subcellular localization to melanosomes.

      GOterm: GO:0032402 (melanosome transport)

      FunctionalEvidence: Exogenously expressed GPR143 in COS-7 cells forms protein-protein interactions with heterotrimeric G-proteins that can be co-immunoprecipitated (Figure 2). This was validated with endogenous GPR143 (Figure 3). GPR143 shows subcellular localization not to the plasma membrane but to melanosomes (Figures 4, 6).

      FunctionalHPO: HP:0005592 (Giant melanosomes in melanocytes), severely reduced microtubule-based motility in melanosomes

      HumanPhenotype: HP:0005592 (Giant melanosomes in melanocytes), HP:0007894 (Hypopigmentation of the fundus), severely reduced microtubule-based motility in melanosomes, Giant melanosomes in retinal pigment epithelial cells

      PhenotypeEvidence: This evidence is consistent with the melanocyte trafficking defects characteristic of human patients.

    1. The ocular albinism type 1 (OA1) G-protein-coupled receptor functions with MART-1 at early stages of melanogenesis to control melanosome identity and composition

      PMID: 19717472

      Gene: GPR143

      HGNC: 20145

      Disease: X-linked recessive ocular albinism

      MONDO: 0021019

      InheritancePattern: X-linked recessive

      Prevalence: Ocular albinism has an estimated prevalence between 1 in 111,000 and 1 in 1,000,000 live births (PMID: 35495622)

      Penetrance: Fully penetrant in males, with onset in infancy. Most female carriers appear to be unaffected.

    1. Case#: Preising_2001_Patient_IV.1, male, age 3 months at time of diagnosis, family ethnicity described as White

      CasePresentingHPOs: HP:0006934 (Congenital nystagmus), HP:0012805 (Iris transillumination defect), HP:0007894 (Hypopigmentation of the fundus), HP:0001104 (Macular hypoplasia), HP:0007663 (Reduced visual acuity), HP:0030463 (Asymmetrical distribution of flash visual evoked potentials), HP:0025551 (Optic nerve misrouting)

      CaseHPOFreeText: The proband and his family members have been diagnosed with congenital nystagmus.

      CaseNotHPOs: HP:0009887 (Abnormality of hair pigmentation), HP:0001000 (Abnormality of skin pigmentation)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: The patients were initially genotyped by SSCP of PCR products from each exon, revealing an abnormality in exon 6.

      CaseMethod1: SSCP

      CaseMethod2: Sanger sequencing

      CaseGenotypingMethod: The proband was initially genotyped by SSCP of PCR products from each exon, revealing an abnormality in exon 6, followed by Sanger sequencing and restriction enzyme analysis by Tsp509I digest of PCR products from all family members.

      Variant: The proband harbors the NM_000273.3(GPR143):c.756_767+2del variant in the hemizygous state.

      ClinVar: 98643

      gnomAD: This variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_000273.3(GPR143):c.756_767+2del is a 14-bp deletion variant removing the 3' end of exon 6 and the canonical splice donor site, and has been shown to trigger aberrant splicing that leads to frameshift at codon 252 and premature termination at codon 259 (Figure 4C).

      CaseAddInfo: The proband is part of a family with at least 3 affected generations showing a pattern of X-linked inheritance, including a similarly affected maternal uncle.

      CasePMIDs: N/A