21 Matching Annotations
  1. Oct 2026
    1. In a sibling pair from a consanguineous marriage (family B) and in a sibling pair from a nonconsanguineous family (family A), we identified large homozygous regions on chromosome 10 (11 Mb and 26 Mb, respectively) (Figure 1A). The common 26 Mb homozygous region in the sibs from family A was the largest homozygous region (SNP boundaries SNP_A-2260521 and SNP_A-1892358); the second, third, and fourth largest regions measured 8, 4.3, and 4.2 Mb. The overlapping 11 Mb homozygous region in the affected sibs of family B was the second largest homozygous region (SNP boundaries SNP_A-2003359 and SNP_A-1804692). The largest region in this family spanned 25 Mb; the third and fourth largest regions measured 10 and 6 Mb. The overlapping homozygous region in both families spanned the PDE6C gene but no other obvious candidate genes (Figure 1A; see also Table S1 available online). These regions were not found in other patients.

      Case#: Thiadens_2009_Family_A_Proband_AII-2, male, age 6 years at onset and 51 years at the time of report, sites of treatment listed as the Netherlands, Belgium, U.K., or Canada

      CasePresentingHPOs: HP:0030534 (Abnormal best corrected visual acuity test), HP:0000613 (Photophobia), HP:0000639 (Nystagmus), HP:0011003 (High myopia), HP:0000551 (Color vision defect, described as severe), HP:0030825 (Absent foveal reflex), HP:0007703 (Abnormality of retinal pigmentation, described as mild), HP:0030465 (Undetectable light-adapted electroretinogram)

      CaseHPOFreeText: The proband and affected family member were previously diagnosed with early onset autosomal recessive cone dystrophy. The proband had onset by age 6 years.

      CaseNotHPOs: HP:0007769 (Peripheral retinal degeneration)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Affected and unaffected family members were initially subjected to homozygosity mapping based on Affymetrix GeneChIP SNP analysis, identifying an 11-Mb region of homozygosity shared with another unrelated family.

      CaseMethod1: homozygosity mapping

      CaseMethod2: screening of the 22 exons and flanking regions of PDE6C (the only strong candidate gene) using Sanger sequencing

      CaseGenotypingMethod: Affected and unaffected family members were initially subjected to homozygosity mapping based on Affymetrix GeneChIP SNP analysis, identifying an 11-Mb region of homozygosity shared with another unrelated family. The clear candidate gene, PDE6C, was then subjected to Sanger sequencing-based screening of the 22 exons and flanking regions.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.85C>T (p.Arg29Trp) variant in the homozygous state.

      ClinVar ID: 8763

      gnomAD: The NM_006204.4(PDE6C):c.85C>T (p.Arg29Trp) variant is found in gnomAD v2.1.1 at a frequency of 0.00008009 (2/24972) in the African / African-American population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/10-95372567-C-T

      VariantEvidence: NM_006204.4(PDE6C):c.85C>T (p.Arg29Trp) is a missense variant that does not have experimental evidence of a functional effect on the protein product. However, it has been reported in similarly affected individuals in other studies (PMID: 21127010, PMID: 30080950).

      CaseAddInfo: The patient's affected sibling shares the same homozygous genotype, while the parents are unaffected and unrelated at least during the last 3 generations.

      CasePMIDs: N/A

    2. Homozygosity Mapping Reveals PDE6C Mutations in Patients with Early-Onset Cone Photoreceptor Disorders

      PMID: 19615668

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    3. complete achromatopsia (families C

      Case#: Thiadens_2009_Family_D_Proband_DII-1, female, age 12 years at onset and 37 years at the time of report, sites of treatment listed as the Netherlands, Belgium, U.K., or Canada

      CasePresentingHPOs: HP:0030534 (Abnormal best corrected visual acuity test), HP:0000613 (Photophobia, described as severe), HP:0000639 (Nystagmus), HP:0031624 (Moderate myopia), HP:0000551 (Color vision defect, described as severe), HP:0030825 (Absent foveal reflex), HP:0030465 (Undetectable light-adapted electroretinogram)

      CaseHPOFreeText: The proband and affected family member were previously diagnosed with complete achromatopsia. The proband had onset by age 12 years.

      CaseNotHPOs: HP:0007769 (Peripheral retinal degeneration)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in this family appears to have been limited to phenotype analysis.

      CaseMethod1: screening of the 22 exons and flanking regions of PDE6C (candidate gene) using Sanger sequencing

      CaseMethod2: N/A

      CaseGenotypingMethod: Affected and unaffected family members were subjected to Sanger sequencing-based screening of the 22 exons and flanking regions of PDE6C.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.633G>C (p.Glu211Asp) and NM_006204.4(PDE6C):c.1363A>G (p.Met455Val) variants in the compound heterozygous state.

      ClinVar ID: 8768, 8767

      gnomAD: Neither variant was found in gnomAD v2.1.1.

      VariantEvidence: NM_006204.4(PDE6C):c.1363A>G (p.Met455Val) is a missense variant that does not have experimental evidence of a functional effect on the protein product. NM_006204.4(PDE6C):c.633G>C (p.Glu211Asp) is not a missense variant but rather a substitution of the last base pair of exon 2 that is predicted to disrupt the splice donor site.

      CaseAddInfo: The patient's parents are apparently unaffected carriers. Her similarly affected sibling shares the same compound heterozygous genotype.

      CasePMIDs: N/A

    1. index case

      Case#: Weisschuh_2018_Patient_8, sex unreported, age 35 years at time of report, likely from Europe or of European descent

      CasePresentingHPOs: HP:0030465 (Undetectable light-adapted electroretinogram), HP:0030534 (Abnormal best corrected visual acuity test), HP:0000551 (Color vision defect), HP:0000613 (Photophobia)

      CaseHPOFreeText: The proband has been previously diagnosed with achromatopsia.

      CaseNotHPOs: HP:0030469 (Abnormal dark-adapted electroretinogram)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: The patient was previously genotyped by Sanger sequencing of CNGB3, CNGA3, and GNAT2.

      CaseMethod1: next-generation sequencing of PDE6C and possibly other loci

      CaseMethod2: screening of the 22 exons and flanking regions of PDE6C (the only strong candidate gene) using Sanger sequencing

      CaseGenotypingMethod: The proband has been genotyped by Sanger sequencing of CNGB3, CNGA3, GNAT2, and PDE6C, as well as next-generation sequencing of PDE6C and possibly other loci.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.78del (p.Lys27fs) and NM_006204.4(PDE6C):c.775C>T (p.Arg259Ter) variants in the compound heterozygous state.

      ClinVar ID: 487693, 487691

      gnomAD: The NM_006204.4(PDE6C):c.78del (p.Lys27fs) variant was not found in gnomAD v2.1.1. The NM_006204.4(PDE6C):c.775C>T (p.Arg259Ter) variant is found in gnomAD v2.1.1 at a frequency of 0.00001759 (2/113724) in the European (non-Finnish) population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/10-95381740-C-T

      VariantEvidence: NM_006204.4(PDE6C):c.775C>T (p.Arg259Ter) is a nonsense variant in exon 4 of 22 that is predicted to trigger nonsense mediated decay or to at least truncate the C-terminal 70% of the protein product. NM_006204.4(PDE6C):c.78del (p.Lys27fs) is a frameshift variant in exon 1 of 12 that is predicted to trigger nonsense mediated decay or to at least truncate the C-terminal 97% of the protein product.

      CaseAddInfo: N/A

      CasePMIDs: N/A

    2. biallelic

      Case#: Weisschuh_2018_Patient_3, sex unreported, age 17 years at time of report, likely from Europe or of European descent

      CasePresentingHPOs: HP:0030465 (Undetectable light-adapted electroretinogram), HP:0000613 (Photophobia), HP:0000639 (Nystagmus)

      CaseHPOFreeText: The proband has been previously diagnosed with achromatopsia.

      CaseNotHPOs: HP:0030469 (Abnormal dark-adapted electroretinogram)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: The patient was previously genotyped by Sanger sequencing of CNGB3, CNGA3, and GNAT2.

      CaseMethod1: next-generation sequencing of PDE6C and possibly other loci

      CaseMethod2: screening of the 22 exons and flanking regions of PDE6C (the only strong candidate gene) using Sanger sequencing

      CaseGenotypingMethod: The proband has been genotyped by Sanger sequencing of CNGB3, CNGA3, GNAT2, and PDE6C, as well as next-generation sequencing of PDE6C and possibly other loci.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.1579C>T (p.Arg527Ter) variant in the homozygous state.

      ClinVar ID: 487692

      gnomAD: The NM_006204.4(PDE6C):c.1579C>T (p.Arg527Ter) variant is found in gnomAD v2.1.1 at a frequency of 0.0002603 (9/34574) in the Latino / Admixed-American population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/10-95399923-C-T

      VariantEvidence: NM_006204.4(PDE6C):c.1579C>T (p.Arg527Ter) is a nonsense variant in exon 12 of 22 that is predicted to trigger nonsense mediated decay or to at least truncate the C-terminal 39% of the protein product.

      CaseAddInfo: N/A

      CasePMIDs: N/A

    3. Mutations in the gene PDE6C encoding the catalytic subunit of the cone photoreceptor phosphodiesterase in patients with achromatopsia

      PMID: 30080950

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    1. Visually impaired rhesus macaques show signs of achromatopsia.

      ExperimentName: This macaque model harbors a homozygous loss-of-function variant in PDE6C.

      NonHumanModel: Macaca mulatta

      GeneAlteration: The model animals are homozygous for a missense variant, p.Arg565Gln, which is shown to cause a decrease in enzymatic activity.

      ModelPhenotype: HP:0007663 (Reduced visual acuity, particularly in well illuminated settings where unaffected animals led them by the hand), HP:0001483 (Eye poking), HP:0030465 (Undetectable light-adapted electroretinogram), normal dark-adapted ERG, HP:0007401 (Macular atrophy), HP:0011504 (Bull's eye maculopathy), HP:0030619 (Reduced OCT-measured foveal thickness), HP:0030610 (Photoreceptor outer segment loss on macular OCT), HP:0030609 (Photoreceptor layer loss on macular OCT)

      HumanPhenotype: HP:0030465 (Undetectable light-adapted electroretinogram), HP:0030534 (Abnormal best corrected visual acuity test), HP:0000551 (Color vision defect), HP:0000613 (Photophobia), HP:0000639 (Nystagmus), HP:0007401 (Macular atrophy), HP:0000545 (Myopia)

      ModelEvidence: This is a naturally occurring macaque model that matches the autosomal recessive mode of inheritance from the human patients (Figure 7) and exhibits reduced visual acuity (Supplemental Video 1), lack of light-adapted ERG responses and normal dark-adapted ERG responses (Figures 1A-1E, Figure 2). The affected animals also exhibit progressive macular atrophy consistent with achromatopsia (Figure 3). Reduced foveal thickness was also observed (Figures 4A, 4B), as well as thinning of the outer nuclear layer and photoreceptor outer segments (Figures 5A, 5B).

      ModelVariant: This model did not introduce a disease-associated variant known from an affected human patient, but rather studied a naturally occurring variant disrupting the PDE6C locus.

    1. Decreased catalytic activity and altered activation properties of PDE6C mutants associated with autosomal recessive achromatopsia

      PMID: 21127010

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    1. c.481–12T>A and c.1483–2A>G in family CHRO 9

      Case#: Chang_2009_Family_CHRO9_Proband_II:3, female, age 26 years at time of report, family origin not described

      CasePresentingHPOs: HP:0000613 (Photophobia), HP:0003593 (Infantile onset), HP:0001141 (Severely reduced visual acuity), HP:0011003 (High myopia), HP:0000551 (Color vision defect, described as complete lack of color discrimination), HP:0000603 (Central scotoma), HP:0030465 (Undetectable light-adapted electroretinogram), HP:0030479 (Abnormal amplitude of light-adapted flicker electroretinogram, described as extinguished), HP:0007401 (Macular atrophy)

      CaseHPOFreeText: The proband and an affected family member were previously diagnosed with achromatopsia.

      CaseNotHPOs: HP:0030469 (Abnormal dark-adapted electroretinogram)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Affected and unaffected family members were initially subjected to genotyping of the CNGA3, GNGB3, and GNAT2 loci, confirming absence of causal variants in these known achromatopsia-related genes.

      CaseMethod1: Sanger sequencing of CNGA3, GNGB3, and GNAT2

      CaseMethod2: Sanger sequencing of the 22 exons and flanking regions of PDE6C

      CaseGenotypingMethod: CNGA3, GNGB3, and GNAT2 were previously screened / known not to harbor causal variants for achromatopsia. The family members were then subjected to Sanger sequencing of the 22 exons and flanking regions of PDE6C.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.481-12T>A and NM_006204.4(PDE6C):c.1483-2A>G variants in the compound heterozygous state.

      ClinVar ID: 8770, 8771

      gnomAD: The NM_006204.4(PDE6C):c.481-12T>A variant was not found in gnomAD v2.1.1. The NM_006204.4(PDE6C):c.1483-2A>G variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_006204.4(PDE6C):c.481-12T>A is an intronic variant that has been subjected to a mini-gene assay in COS7 cells and triggers a fully penetrant splicing defect (use of a cryptic splice site 10 nucleotides upstream, resulting in a frameshift encoding p.Asn161fsX169, Figure S5A). NM_006204.4(PDE6C):c.1483-2A>G is a canonical splice site variant that has been subjected to a mini-gene assay in COS7 cells and triggers a fully penetrant splicing defect (exon 12 skipping, resulting in an in-frame deletion encoding p.495_543del49, Figure S5B).

      CaseAddInfo: The patient has an affected sister who shares the same compound heterozygous genotype, while the parents and one other sibling are each unaffected carriers.

      CasePMIDs: N/A

    2. A homologous genetic basis of the murine cpfl1 mutant and human achromatopsia linked to mutations in the PDE6C gene

      PMID: 19887631

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    3. c.1805A>T/p.His602Leu and c.2368G>A/p.Glu790Lys in family CHRO 102

      Case#: Chang_2009_Family_CHRO102_Proband_II:1, male, age and family origin not described

      CasePresentingHPOs: HP:0011516 (Achromatopsia)

      CaseHPOFreeText: The proband and an affected family member were previously diagnosed with achromatopsia.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Affected and unaffected family members were initially subjected to genotyping of the CNGA3, GNGB3, and GNAT2 loci, confirming absence of causal variants in these known achromatopsia-related genes.

      CaseMethod1: Sanger sequencing of CNGA3, GNGB3, and GNAT2

      CaseMethod2: Sanger sequencing of the 22 exons and flanking regions of PDE6C

      CaseGenotypingMethod: CNGA3, GNGB3, and GNAT2 were previously screened / known not to harbor causal variants for achromatopsia. The family members were then subjected to Sanger sequencing of the 22 exons and flanking regions of PDE6C.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.2368G>A (p.Glu790Lys) and NM_006204.4(PDE6C):c.1805A>T (p.His602Leu) variants in the compound heterozygous state.

      ClinVar ID: 8769, 8772

      gnomAD: The NM_006204.4(PDE6C):c.2368G>A (p.Glu790Lys) variant was not found in gnomAD v2.1.1. The NM_006204.4(PDE6C):c.1805A>T (p.His602Leu) variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_006204.4(PDE6C):c.2368G>A (p.Glu790Lys) acts in part as an exonic splicing variant that has been expressed in COS7 cells and triggers 40% of transcripts to skip exon 21 and undergo frameshift (Figure S5C). The remaining transcripts encode a missense variant that has been expressed in Sf9 cells and subjected to an enzymatic assay showing approximately 40% loss of activity (Figure 5). NM_006204.4(PDE6C):c.1805A>T (p.His602Leu) is a missense variant that has been expressed in Sf9 cells and subjected to an enzymatic assay showing approximately 90% loss of activity (Figure 5).

      CaseAddInfo: The patient has an affected brother who shares the same compound heterozygous genotype, while the parents and one other sibling are each unaffected carriers.

      CasePMIDs: N/A

    4. Moreover, we show that the spontaneous mouse mutant cpfl1 that features a lack of cone function and rapid degeneration of the cone photoreceptors represents a homologous mouse model for PDE6C associated achromatopsia.

      ExperimentName: The Cpfl1 mouse harbors loss-of-function variants in the Pde6c gene.

      NonHumanModel: Mus musculus

      GeneAlteration: The model animals are homozygous for two different loss-of-function variants predicted to introduce premature stop codons into the Pde6c locus. One is a 116-bp insertion between exons 4 and 5, while the other is a 1-bp deletion in exon 7.

      ModelPhenotype: HP:0008020 (cone dystrophy), HP:0030465 (Undetectable light-adapted electroretinogram), normal dark-adapted ERG, rapid and progressive loss of cone photoreceptors from the photoreceptor layer

      HumanPhenotype: HP:0030465 (Undetectable light-adapted electroretinogram), HP:0030534 (Abnormal best corrected visual acuity test), HP:0000551 (Color vision defect), HP:0000613 (Photophobia), HP:0000639 (Nystagmus), HP:0007401 (Macular atrophy), HP:0000545 (Myopia)

      ModelEvidence: This is a naturally occurring mouse model with lack of light-adapted ERG responses and normal dark-adapted ERG responses (Figure 1). The mice also exhibit rapid and progressive loss of cone photoreceptors from retinal sections (Figure 2).

      ModelVariant: This model did not introduce a disease-associated variant known from an affected human patient, but rather studied naturally occurring variants disrupting the Pde6c locus.

    5. We then extended our mutation screening study to include 24 additional simplex achromatopsia patients that were also prescreened and did not carry mutations in the known achromatopsia genes. Among those 24 patients, we identified one further subject (CHRO 287) with two heterozygous nonsense mutations, c.826C>T/p.Arg276X and c.2457T>A/p.Tyr819X

      Case#: Chang_2009_Family_CHRO287_Proband_II:1, male, age and family origin not described

      CasePresentingHPOs: HP:0011516 (Achromatopsia)

      CaseHPOFreeText: The proband was previously diagnosed with achromatopsia.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: The proband and his parents were initially subjected to genotyping of the CNGA3, GNGB3, and GNAT2 loci, confirming absence of causal variants in these known achromatopsia-related genes.

      CaseMethod1: Sanger sequencing of CNGA3, GNGB3, and GNAT2

      CaseMethod2: Sanger sequencing of the 22 exons and flanking regions of PDE6C

      CaseGenotypingMethod: CNGA3, GNGB3, and GNAT2 were previously screened / known not to harbor causal variants for achromatopsia. The family members were then subjected to Sanger sequencing of the 22 exons and flanking regions of PDE6C.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.826C>T (p.Arg276Ter) and NM_006204.4(PDE6C):c.2457T>A (p.Tyr819Ter) variants in the compound heterozygous state.

      ClinVar ID: 8773, 8774

      gnomAD: The NM_006204.4(PDE6C):c.826C>T (p.Arg276Ter) variant is found in gnomAD v2.1.1 at a frequency of 0.00006152 (1 allele / 16256 total alleles) in the African / African-American population, with 0 homozygotes. The NM_006204.4(PDE6C):c.2457T>A (p.Tyr819Ter) variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_006204.4(PDE6C):c.826C>T (p.Arg276Ter) is a nonsense variant in exon 4 of 22 and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 68% of the protein product. NM_006204.4(PDE6C):c.2457T>A (p.Tyr819Ter) is a nonsense variant in exon 21 of 22 and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 5% of the protein product.

      CaseAddInfo: The patient has an affected brother who shares the same compound heterozygous genotype, while the parents and one other sibling are each unaffected carriers.

      CasePMIDs: N/A

    6. another subject (CHRO 572) with a homozygous 1-bp insertion, c.1682_83insA/p.Tyr561X in PDE6C

      Case#: Chang_2009_Family_CHRO572_Proband_II:1, male, age and family origin not described

      CasePresentingHPOs: HP:0011516 (Achromatopsia)

      CaseHPOFreeText: The proband was previously diagnosed with achromatopsia.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: The proband and his family members were initially subjected to genotyping of the CNGA3, GNGB3, and GNAT2 loci, confirming absence of causal variants in these known achromatopsia-related genes.

      CaseMethod1: Sanger sequencing of CNGA3, GNGB3, and GNAT2

      CaseMethod2: Sanger sequencing of the 22 exons and flanking regions of PDE6C

      CaseGenotypingMethod: CNGA3, GNGB3, and GNAT2 were previously screened / known not to harbor causal variants for achromatopsia. The family members were then subjected to Sanger sequencing of the 22 exons and flanking regions of PDE6C.

      Variant: The proband harbors the NM_006204.4(PDE6C):c.1682dup (p.Tyr561Ter) variant in the homozygous state.

      ClinVar ID: 8775

      gnomAD: The NM_006204.4(PDE6C):c.1682dup (p.Tyr561Ter) variant was not found in gnomAD v2.1.1.

      VariantEvidence: NM_006204.4(PDE6C):c.1682dup (p.Tyr561Ter) is a nonsense variant in exon 13 of 22 and is predicted to trigger nonsense-mediated decay or to at least truncate the C-terminal 35% of the protein product.

      CaseAddInfo: The patient's parents and sister are each unaffected heterozygous carriers of the variant.

      CasePMIDs: N/A

    1. PDE6C hydrolyzed cGMP with a Km of 65 ± 6 μm and kcat of 4400 ± 300 s−1 (Fig. 7A).

      Selection B- Gene function is consistent with phenotype.

      GOterm: GO:0047555 (3',5'-cyclic-GMP phosphodiesterase activity)

      FunctionalEvidence: Purified PDE6C hydrolyzed cGMP with a Km and kcat slightly lower than trypsin-activated bovine rod PDE6 (Figure 7A).

      FunctionalHPO: HP:0000551 (Color vision defect), HP:0030465 (Undetectable light-adapted electroretinogram)

    2. Characterization of Human Cone Phosphodiesterase-6 Ectopically Expressed in Xenopus laevis Rods

      PMID: 19801642

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    1. Clinical genomics can facilitate countrywide estimation of autosomal recessive disease burden

      PMID: 27124789

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    1. Here, we report that a mutation in the gene encoding a central effector of the phototransduction cascade, cGMP phosphodiesterase 6alpha'-subunit (PDE6alpha'), affects not only the vision but also the survival of cone photoreceptors in zebrafish. We isolated a zebrafish mutant, called eclipse (els), which shows no visual behavior such as optokinetic response (OKR). The cloning of the els mutant gene revealed that a missense mutation occurred in the pde6alpha' gene, resulting in a change in a conserved amino acid. The PDE6 expressed in rod photoreceptors is a heterotetramer comprising two closely related similar hydrolytic alpha and beta subunits and two identical inhibitory gamma subunits, while the PDE6 expressed in cone photoreceptors consists of two homodimers of alpha' subunits, each with gamma subunits. The els mutant displays no visual response to bright light, where cones are active, but shows relatively normal OKR to dim light, where only rods function, suggesting that only the cone-specific phototransduction pathway is disrupted in the els mutant. Furthermore, in the els mutant, cones are selectively eliminated but rods are retained at the adult stage, suggesting that cones undergo a progressive degeneration in the els mutant retinas. Taken together, these data suggest that PDE6alpha' activity is important for the survival of cones in zebrafish.

      ExperimentName: The eclipse / els zebrafish mutant harbors a missense variant in the PDE6C ortholog pde6alpha'.

      NonHumanModel: Danio rerio

      GeneAlteration: The model animals are homozygous for a missense variant p.Met175Arg.

      ModelPhenotype: HP:0008020 (cone dystrophy), HP:0030465 (Undetectable light-adapted electroretinogram), normal dark-adapted ERG, rapid and progressive elimination of cone photoreceptors from adult retinas

      HumanPhenotype: HP:0030465 (Undetectable light-adapted electroretinogram), HP:0030534 (Abnormal best corrected visual acuity test), HP:0000551 (Color vision defect), HP:0000613 (Photophobia), HP:0000639 (Nystagmus), HP:0007401 (Macular atrophy), HP:0000545 (Myopia)

      ModelEvidence: This is a naturally occurring zebrafish model that matches the mode of inheritance from the human patients and exhibits lack of light-adapted ERG responses (Figures 1K, 1M) and normal dark-adapted ERG responses. Optokinetic responses mediated by rod function were normal, while those mediated by cone function were absent (Figure 4). The mice also exhibit rapid and progressive loss of cone photoreceptors from retinal sections (Figures 1G, 1I) and abnormal shape of the photoreceptor outer segment (Figure 1C). Rod markers are maintained while cone markers are absent from adult animals (Figure 4).

      ModelVariant: This model did not introduce a disease-associated variant known from an affected human patient, but rather studied a naturally occurring variant disrupting the PDE6alpha' locus orthologous to human PDE6C.

    2. Mutation of cGMP phosphodiesterase 6alpha'-subunit gene causes progressive degeneration of cone photoreceptors in zebrafish

      PMID: 18824093

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.

    1. Exome Sequencing of 47 Chinese Families with Cone-Rod Dystrophy: Mutations in 25 Known Causative Genes

      PMID: 23776498

      Gene: PDE6C

      HGNC: 8787

      Disease: cone dystrophy 4

      MONDO: 0013129

      InheritancePattern: recessive

      Prevalence: cone dystrophy in general is estimated to have a prevalence of 1 in 40,000 (PMID: 30578485).

      Penetrance: The penetrance of the phenotype among homozygous cases appears to be complete.