RP1-Related Retinopathy

Mendelian MONDO:0800400 Pathograph 8 Show in embeddings browser Retinitis pigmentosa Inherited Retinal Dystrophy

RP1-related retinopathy is an inherited retinal dystrophy caused by pathogenic variants in RP1, encoding a 2,156-amino-acid microtubule-associated protein (MAP) localized to the connecting cilium and axoneme of photoreceptors. RP1 contains an N-terminal doublecortin (DCX) domain and a bifocal (BIF) domain and is required for correct orientation and higher-order stacking of the photoreceptor outer segment discs. RP1 has four exons, with the protein-coding region in the last three; exon 4 alone encodes more than 85% of the protein and harbors most known pathogenic variants. Nearly all known pathogenic variants are nonsense or frameshift changes (truncating variants account for roughly 80% of reported pathogenic RP1 alleles), predicted to truncate the protein by roughly 50-70%. RP1 is unusual among retinal dystrophy genes in causing disease through two distinct genetic mechanisms from the same locus: heterozygous truncating variants clustered in the middle of exon 4 act as dominant-negative alleles, causing autosomal dominant retinitis pigmentosa (adRP); biallelic truncating variants located toward the N- or C-terminal ends of exon 4 cause a distinct, generally more severe autosomal recessive retinitis pigmentosa (arRP) through loss of function, though a subset of biallelic exon-2 missense variants can instead cause a considerably later-onset phenotype. Studies excluding haploinsufficiency as the causative mechanism support a dominant-negative model for the heterozygous middle-exon-4 variants instead. No RP1-specific gene therapy is in clinical trials as of 2026; management is supportive.

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2
Inheritance
4
Pathophys.
9
Phenotypes
8
Pathograph
1
Genes
2
Medical Actions
1
Subtypes
8
References
👪

Inheritance

2
Autosomal dominant HP:0000006
Heterozygous truncating variants clustered in the middle portion of RP1 exon 4 act through a dominant-negative mechanism rather than haploinsufficiency. RP1 accounts for a substantial fraction of autosomal dominant retinitis pigmentosa. Each child of an affected parent has a 50% chance of inheriting the pathogenic variant.
Autosomal dominant inheritance
Show evidence (1 reference)
PMID:33681214 SUPPORT Human Clinical
"some studies have excluded haploinsufficiency and gain-of-function as the causative mechanism of RP1 variants"
Establishes that dominant RP1 disease is not caused by simple haploinsufficiency, supporting a dominant-negative mechanism for heterozygous truncating variants.
Autosomal recessive HP:0000007
Biallelic truncating variants toward the N- or C-terminal ends of RP1 exon 4 cause a distinct, more severe autosomal recessive retinitis pigmentosa through loss of function. Both parents of an affected child are obligate heterozygous carriers; each sibling has a 25% chance of being affected.
Autosomal recessive inheritance
Show evidence (1 reference)
PMID:32565670 SUPPORT Human Clinical
"Biallelic RP1 mutations cause a broad spectrum of retinal disease."
Reports as a finding that biallelic (not simply heterozygous) RP1 variants cause retinal disease, directly evidencing the autosomal recessive inheritance modeled by this node.

Subtypes

1
RP1-Related Recessive Retinopathy MONDO:0800399
Autosomal recessive RP1-related retinitis pigmentosa caused by biallelic truncating variants located toward the N- or C-terminal ends of RP1 exon 4, producing complete loss of functional RP1 protein. This form is generally more severe than the dominant form: a US multicenter cohort had symptom onset ranging 4-30 years of age (mean 14.9, median 13) with macular atrophy common across the cohort, and a separate Brazilian cohort reported diagnosis within the first decade of life with severely affected visual acuity at a young age. Patients carrying at least one exon-2 missense variant can have a considerably later onset than this average.

Pathophysiology

4
Heterozygous RP1 Dominant-Negative Truncation
Heterozygous truncating (nonsense/frameshift) variants clustered in the middle portion of RP1 exon 4 - which alone encodes more than 85% of the protein despite RP1 having four exons total - produce a stable, partially functional truncated protein that retains the N-terminal doublecortin (DCX) domain but loses distal sequence needed for normal regulation. This truncated product co-assembles with wild-type RP1 at the photoreceptor axoneme and interferes with normal microtubule/axoneme organization, a dominant-negative mechanism rather than simple haploinsufficiency. This is the more common RP1 disease mechanism and underlies the majority of RP1-related autosomal dominant RP.
retinal rod cell CL:0000604 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal rod cell (CL:0000604). CL:0000604 is a cell type from the Cell Ontology. retinal cone cell CL:0000573 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal cone cell (CL:0000573). CL:0000573 is a cell type from the Cell Ontology.
RP1 hgnc:10263 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves abnormal RP1 (hgnc:10263). hgnc:10263 is a gene from the HUGO Gene Nomenclature Committee. ⚠ ABNORMAL
Genetic context RP1 hgnc:10263 HUGO Gene Nomenclature Committee (hgnc) Relation: this genetic context concerns this gene This genetic context concerns RP1 (hgnc:10263). hgnc:10263 is a gene from the HUGO Gene Nomenclature Committee. functional_impact_category: DOMINANT_NEGATIVE
Heterozygous middle-exon-4 truncating variants retain the BIF domain and produce an interfering truncated product rather than simply haploinsufficient loss of RP1 protein.
Show evidence (3 references)
PMID:33681214 SUPPORT Human Clinical
"the heterozygous variants will cause retinal degeneration with preserved BIF domain but loss of the unrecognized domain"
Directly supports the dominant-negative model: heterozygous truncations that retain the BIF domain but lose additional distal sequence cause retinal degeneration despite the presence of one normal allele, consistent with an interfering truncated product rather than simple haploinsufficiency.
PMID:33681214 SUPPORT Human Clinical
"For the variants associated with adRP, the truncated production will preserve the BIF domain and may cause disease via a dominant-negative effect"
Directly supports the dominant-negative (rather than haploinsufficient) mechanism for heterozygous RP1 truncating variants preserving the BIF domain.
PMID:33681214 SUPPORT Human Clinical
"the middle portion from c.1981 (p.661) to c.2749 (p.917)"
Provides the precise coding-sequence/protein coordinates defining the middle-exon-4 region where heterozygous truncations act as dominant-negative alleles, refining the "middle portion" claim made by this node.
Biallelic RP1 Loss
Biallelic truncating variants located toward the N- or C-terminal ends of RP1 exon 4 (distinct from the middle-clustered dominant variants) produce complete loss of functional RP1 protein when present on both alleles. Heterozygous carriers of these same terminal variants are clinically unaffected, confirming that a single functional RP1 allele is sufficient for normal photoreceptor structure and that recessive disease requires complete loss rather than a dominant-negative product.
retinal rod cell CL:0000604 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal rod cell (CL:0000604). CL:0000604 is a cell type from the Cell Ontology. retinal cone cell CL:0000573 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal cone cell (CL:0000573). CL:0000573 is a cell type from the Cell Ontology.
RP1 hgnc:10263 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves absent RP1 (hgnc:10263). hgnc:10263 is a gene from the HUGO Gene Nomenclature Committee. ∅ ABSENT
Genetic context RP1 hgnc:10263 HUGO Gene Nomenclature Committee (hgnc) Relation: this genetic context concerns this gene This genetic context concerns RP1 (hgnc:10263). hgnc:10263 is a gene from the HUGO Gene Nomenclature Committee. functional_impact_category: LOSS_OF_FUNCTION
Biallelic N-/C-terminal truncating variants produce complete loss of functional RP1 protein; a single functional allele is sufficient for normal photoreceptor structure, so disease requires loss of both alleles.
Show evidence (2 references)
PMID:32005865 SUPPORT Human Clinical
"They had classic retinitis pigmentosa with diagnosis at the first decade of life. The visual acuities were severely affected at a young age."
Documents the severe, early-onset phenotype resulting from biallelic RP1 loss-of-function variants, consistent with complete loss of RP1 function.
PMID:33681214 SUPPORT Human Clinical
"Heterozygous truncations alone in the N- and C- terminals were unlikely pathogenic."
A described negative control: this cohort's single heterozygous N-/C-terminal truncations were not enriched in RP patients and were judged unlikely pathogenic, directly supporting the claim that one functional RP1 allele is sufficient and that biallelic loss is required for recessive disease.
Photoreceptor Axoneme Disorganization
RP1 is a photoreceptor-specific microtubule-associated protein located in the connecting cilium and axoneme, where it controls the length and stability of the axoneme and is required for correct orientation and higher-order stacking of outer segment discs. Loss of functional RP1 (via either the dominant-negative or recessive loss-of-function mechanism) disrupts this scaffolding role, producing misoriented, disorganized outer segment discs.
retinal rod cell CL:0000604 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal rod cell (CL:0000604). CL:0000604 is a cell type from the Cell Ontology.
cilium assembly GO:0060271 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves abnormal cilium assembly (GO:0060271). GO:0060271 is a biological process from the Gene Ontology. ⚠ ABNORMAL
ciliary transition zone GO:0035869 Gene Ontology (GO) Relation: this pathophysiological event involves this cellular component This pathophysiological event involves ciliary transition zone (GO:0035869). GO:0035869 is a cellular component from the Gene Ontology.
Show evidence (2 references)
PMID:15269252 SUPPORT Model Organism
"Disruption of the Rp1 gene in mice causes misorientation of outer segment discs, suggesting a role for RP1 in outer segment organization."
Establishes RP1's structural role in outer segment disc organization using the Rp1 knockout mouse model; loss of RP1 causes disc misorientation, the direct structural consequence modeled by this node.
PMID:15269252 SUPPORT Model Organism
"we show that the RP1 protein is part of the photoreceptor axoneme"
Establishes the subcellular localization of RP1 to the connecting cilium/axoneme, the structure disrupted in this node.
Rod Photoreceptor Apoptosis
Progressive structural disorganization of the outer segment from dysfunctional RP1 ultimately drives rod photoreceptor apoptosis, the hallmark rod-predominant degeneration of retinitis pigmentosa producing nyctalopia and progressive peripheral visual field loss. Secondary cone degeneration follows as rods are lost. The recessive form progresses far more rapidly and with earlier macular involvement than the dominant form.
retinal rod cell CL:0000604 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves retinal rod cell (CL:0000604). CL:0000604 is a cell type from the Cell Ontology.
neuron apoptotic process GO:0051402 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased neuron apoptotic process (GO:0051402). GO:0051402 is a biological process from the Gene Ontology. ↑ INCREASED
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
Orphanet establishes progressive photoreceptor loss as the defining pathophysiological feature of retinitis pigmentosa, including RP1-RP.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for RP1-Related Retinopathy Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

9
Eye 4
Abnormal Electroretinogram VERY_FREQUENT HP:0000512 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Abnormal electroretinogram (HP:0000512). HP:0000512 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0000512 | Abnormal electroretinogram | Very frequent (99-80%)"
Orphanet records abnormal ERG as a very frequent finding in RP.
Reduced Visual Acuity VERY_FREQUENT HP:0007663 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Reduced visual acuity (HP:0007663). HP:0007663 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
PMID:32005865 SUPPORT Human Clinical
"They had classic retinitis pigmentosa with diagnosis at the first decade of life. The visual acuities were severely affected at a young age."
Documents the severe, early-onset visual acuity loss characteristic of recessive RP1-RP in a biallelic-variant cohort.
PMID:33681214 SUPPORT Human Clinical
"patients with arRP due to biallelic RP1 variants had a significantly earlier age at onset"
Genotype-phenotype comparison in this pooled cohort found significantly earlier age at onset for biallelic (recessive) RP1 patients than for heterozygous (dominant) RP1 patients, a quantified statistic supporting the earlier/more-severe recessive course modeled by this node.
Macular Atrophy VERY_FREQUENT HP:0007401 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Macular atrophy (HP:0007401). HP:0007401 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
PMID:32565670 SUPPORT Human Clinical
"Macular atrophy was a common feature across the cohort."
Directly reports macular atrophy as a common feature (FREQUENT band) across this biallelic RP1 cohort.
PMID:32005865 SUPPORT Human Clinical
"Macular atrophy was found in almost all patients"
Reports macular atrophy in almost all patients of this biallelic RP1 cohort, mapping to the VERY_FREQUENT band under the DisMech qualitative frequency mapping.
Progressive Visual Loss VERY_FREQUENT HP:0000529 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Progressive visual loss (HP:0000529). HP:0000529 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
Orphanet establishes progressive photoreceptor loss over decades as the defining natural history of retinitis pigmentosa, including RP1-RP.
Other 5
Progressive Night Blindness VERY_FREQUENT HP:0007675 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Progressive night blindness (HP:0007675). HP:0007675 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
ORPHA:791 SUPPORT Human Clinical
"HP:0007675 | Progressive night blindness | Very frequent (99-80%)"
Orphanet records progressive night blindness as a very frequent feature of retinitis pigmentosa.
PMID:20301590 SUPPORT Other
"Describe the clinical characteristics of nonsyndromic retinitis pigmentosa"
GeneReviews' clinical-characteristics scope for nonsyndromic RP, including RP1-related forms, covers presenting symptoms such as nyctalopia.
Peripheral Visual Field Loss FREQUENT HP:0007994 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Peripheral visual field loss (HP:0007994). HP:0007994 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0007994 | Peripheral visual field loss | Frequent (79-30%)"
Orphanet records peripheral visual field loss as a frequent phenotype of retinitis pigmentosa.
Bone Spicule Pigmentation of the Retina VERY_FREQUENT Spicular pigmentation of the retina HP:0007737 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Bone spicule pigmentation of the retina, annotated with Spicular pigmentation of the retina (HP:0007737). HP:0007737 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0007737 | Bone spicule pigmentation of the retina | Very frequent (99-80%)"
Orphanet records bone spicule retinal pigmentation as a very frequent finding in retinitis pigmentosa.
Attenuation of Retinal Blood Vessels FREQUENT HP:0007843 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Attenuation of retinal blood vessels (HP:0007843). HP:0007843 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0007843 | Attenuation of retinal blood vessels | Frequent (79-30%)"
Orphanet records retinal vascular attenuation as a frequent feature of RP.
Optic Disc Pallor FREQUENT HP:0000543 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Optic disc pallor (HP:0000543). HP:0000543 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0000543 | Optic disc pallor | Frequent (79-30%)"
Orphanet records optic disc pallor as a frequent finding in RP.
🧬

Genetic Associations

1
RP1 pathogenic variants (Causative)
Gene: RP1 hgnc:10263 HUGO Gene Nomenclature Committee (hgnc) Relation: this disease-associated gene is this gene This disease-associated gene is RP1 (hgnc:10263). hgnc:10263 is a gene from the HUGO Gene Nomenclature Committee.
Autosomal dominant Autosomal recessive
Show evidence (1 reference)
PMID:15269252 SUPPORT Model Organism
"RP1 is a MAP. Given the specific expression of RP1 in photoreceptors, RP1 is thus the first photoreceptor-specific MAP to be identified."
Establishes RP1 as a photoreceptor-specific microtubule-associated protein, the functional basis for its role in RP.
💊

Medical Actions

2
Low Vision Rehabilitation
Action: supportive careNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is supportive care (NCIT:C15747). NCIT:C15747 is a clinical intervention from the NCI Thesaurus. Ontology label: Supportive Care NCIT:C15747
Low vision aids, orientation and mobility training, and adaptive technology are the mainstay of management for RP1-related RP, particularly important for the early and severe visual loss of recessive disease.
Target Phenotypes: Progressive visual loss HP:0000529 Human Phenotype Ontology (HP) Relation: this treatment targets this phenotype This treatment targets Progressive visual loss (HP:0000529). HP:0000529 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
ORPHA:791 SUPPORT Human Clinical
"Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
Progressive visual impairment in RP justifies ongoing low-vision rehabilitation as the primary symptomatic management strategy.
PMID:20301590 SUPPORT Other
"Provide a brief summary of management of nonsyndromic retinitis pigmentosa"
GeneReviews includes a management summary for nonsyndromic RP, including RP1-related forms, of which low vision rehabilitation is a core component.
Genetic Counseling
Action: Genetic CounselingNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Genetic Counseling (NCIT:C15240). NCIT:C15240 is a clinical intervention from the NCI Thesaurus. NCIT:C15240
Essential given RP1's unusual dual inheritance pattern: counseling must distinguish the 50% recurrence risk and generally milder course of dominant disease from the 25% recurrence risk and generally more severe course of recessive disease, which depend on where in exon 4 (and, for biallelic variants, whether an exon-2 missense allele is involved) the family's variant(s) fall.
Show evidence (2 references)
PMID:22317909 SUPPORT Human Clinical
"RP1 is one of the earliest identified disease genes in RP with mutations in this gene known to act both recessively and dominantly although the mutational mechanism remains unclear."
RP1's dual inheritance pattern, with mechanism-dependent recurrence risk, underscores the need for genotype-specific genetic counseling.
PMID:20301590 SUPPORT Other
"Inform genetic risk assessment of family members of a proband with nonsyndromic retinitis pigmentosa"
GeneReviews explicitly scopes this overview to inform genetic risk assessment of family members, the core purpose of genetic counseling modeled by this node.
🔬

Diagnosis

2
Full-Field Electroretinography (ERG)
Full-field ERG is the diagnostic cornerstone for RP1-related RP, showing a rod-cone pattern of dysfunction that is milder and later-onset in dominant disease than in recessive disease.
electroretinogram procedure NCIT:C101217 NCI Thesaurus (NCIT)
Show evidence (1 reference)
ORPHA:791 SUPPORT Human Clinical
"HP:0000512 | Abnormal electroretinogram | Very frequent (99-80%)"
The very high frequency of abnormal ERG in RP supports ffERG as a core diagnostic investigation for RP1-RP.
Molecular Genetic Testing
Sequencing of RP1's coding exons - particularly exon 4, which alone encodes more than 85% of the protein and harbors most known pathogenic variants - identifies the truncating variants responsible for both dominant and recessive disease. Variant position within exon 4 (middle vs. terminal) and zygosity together determine expected inheritance pattern and prognosis, informing genetic counseling.
genetic testing NCIT:C15709 NCI Thesaurus (NCIT)
Show evidence (2 references)
PMID:33681214 SUPPORT Human Clinical
"RP1 is listed as the top seventh of the most frequently implicated genes in inherited retinal disease based on a large cohort."
Supports the clinical value of including RP1 in molecular genetic testing panels for inherited retinal disease given its high frequency.
PMID:20301590 SUPPORT Other
"Provide an evaluation strategy to identify the genetic cause of nonsyndromic retinitis pigmentosa in a proband"
GeneReviews frames molecular genetic testing as the evaluation strategy for identifying the genetic cause of nonsyndromic RP, including RP1.
{ }

Source YAML

click to show
name: RP1-Related Retinopathy
creation_date: "2026-08-13T21:00:00Z"
category: Mendelian
description: >-
  RP1-related retinopathy is an inherited retinal dystrophy caused by pathogenic
  variants in RP1, encoding a 2,156-amino-acid microtubule-associated protein
  (MAP) localized to the connecting cilium and axoneme of photoreceptors. RP1
  contains an N-terminal doublecortin (DCX) domain and a bifocal (BIF) domain
  and is required for correct orientation and higher-order stacking of the
  photoreceptor outer segment discs. RP1 has four exons, with the protein-coding
  region in the last three; exon 4 alone encodes more than 85% of the protein and
  harbors most known pathogenic variants. Nearly all known pathogenic variants are
  nonsense or frameshift changes (truncating variants account for roughly 80% of
  reported pathogenic RP1 alleles), predicted to truncate the protein by roughly
  50-70%. RP1 is unusual among retinal dystrophy genes in causing disease
  through two distinct genetic mechanisms from the same locus: heterozygous
  truncating variants clustered in the middle of exon 4 act as dominant-negative
  alleles, causing autosomal dominant retinitis pigmentosa (adRP); biallelic
  truncating variants located toward the N- or C-terminal ends of exon 4 cause a
  distinct, generally more severe autosomal recessive retinitis pigmentosa
  (arRP) through loss of function, though a subset of biallelic exon-2 missense
  variants can instead cause a considerably later-onset phenotype. Studies
  excluding haploinsufficiency as the causative mechanism support a
  dominant-negative model for the heterozygous middle-exon-4 variants instead.
  No RP1-specific gene therapy is in clinical trials as of 2026; management is
  supportive.
disease_term:
  preferred_term: RP1-related dominant retinopathy
  term:
    id: MONDO:0800400
    label: RP1-related dominant retinopathy
synonyms:
- Retinitis pigmentosa 1
- RP1
- autosomal dominant retinitis pigmentosa due to RP1
- RP1-associated retinal dystrophy
parents:
- Retinitis pigmentosa
- Inherited Retinal Dystrophy
notes: >-
  MONDO's own free-text definitions for the two gene-series terms used here
  (MONDO:0800399 "RP1-related recessive retinopathy" and MONDO:0800400
  "RP1-related dominant retinopathy") appear to have their `def:` fields swapped
  relative to their labels (the "recessive" term's definition text describes
  dominant inheritance and vice versa) - the `is_a` axioms (autosomal recessive
  disease vs. autosomal dominant disease) are internally consistent with the
  labels and were used as the source of truth here, not the free-text defs. The
  older, more general MONDO:0008377 "retinitis pigmentosa 1" (xref OMIM:180100)
  predates the split into dominant/recessive gene-series terms and was not used
  as the primary anchor. One Chinese cohort attributed roughly 2% of RP cases to
  RP1 (a single-gene share broadly comparable to other major RP genes across
  ethnicities). Disease severity generally differs by inheritance: a US
  multicenter cohort of biallelic (recessive) patients had symptom onset
  ranging 4-30 years of age (mean 14.9, median 13) with macular atrophy common
  across the cohort, and a separate Brazilian biallelic cohort reported
  diagnosis within the first decade of life with severe visual acuity loss at a
  young age; within the US cohort, patients carrying at least one exon-2
  missense variant had a considerably later onset than the biallelic-RP1
  average. Dominant RP1-RP is generally considered comparatively milder and
  later in onset than the recessive form, though a precisely quantified age
  range for the dominant form specifically was not found in the sources used
  here.
has_subtypes:
- name: Recessive
  display_name: RP1-Related Recessive Retinopathy
  subtype_term:
    preferred_term: RP1-related recessive retinopathy
    term:
      id: MONDO:0800399
      label: RP1-related recessive retinopathy
  description: >-
    Autosomal recessive RP1-related retinitis pigmentosa caused by biallelic
    truncating variants located toward the N- or C-terminal ends of RP1 exon 4,
    producing complete loss of functional RP1 protein. This form is generally
    more severe than the dominant form: a US multicenter cohort had symptom
    onset ranging 4-30 years of age (mean 14.9, median 13) with macular atrophy
    common across the cohort, and a separate Brazilian cohort reported
    diagnosis within the first decade of life with severely affected visual
    acuity at a young age. Patients carrying at least one exon-2 missense
    variant can have a considerably later onset than this average.

inheritance:
- name: Autosomal dominant
  inheritance_term:
    preferred_term: Autosomal dominant inheritance
    term:
      id: HP:0000006
      label: Autosomal dominant inheritance
  description: >-
    Heterozygous truncating variants clustered in the middle portion of RP1
    exon 4 act through a dominant-negative mechanism rather than
    haploinsufficiency. RP1 accounts for a substantial fraction of autosomal
    dominant retinitis pigmentosa. Each child of an affected parent has a 50%
    chance of inheriting the pathogenic variant.
  evidence:
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "some studies have excluded haploinsufficiency and gain-of-function as the causative mechanism of RP1 variants"
    explanation: >-
      Establishes that dominant RP1 disease is not caused by simple
      haploinsufficiency, supporting a dominant-negative mechanism for
      heterozygous truncating variants.
- name: Autosomal recessive
  inheritance_term:
    preferred_term: Autosomal recessive inheritance
    term:
      id: HP:0000007
      label: Autosomal recessive inheritance
  description: >-
    Biallelic truncating variants toward the N- or C-terminal ends of RP1 exon 4
    cause a distinct, more severe autosomal recessive retinitis pigmentosa
    through loss of function. Both parents of an affected child are obligate
    heterozygous carriers; each sibling has a 25% chance of being affected.
  evidence:
  - reference: PMID:32565670
    reference_title: "Biallelic RP1-associated retinal dystrophies: Expanding the mutational and clinical spectrum"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Biallelic RP1 mutations cause a broad spectrum of retinal disease."
    explanation: >-
      Reports as a finding that biallelic (not simply heterozygous) RP1
      variants cause retinal disease, directly evidencing the autosomal
      recessive inheritance modeled by this node.

pathophysiology:
- name: Heterozygous RP1 Dominant-Negative Truncation
  description: >-
    Heterozygous truncating (nonsense/frameshift) variants clustered in the
    middle portion of RP1 exon 4 - which alone encodes more than 85% of the
    protein despite RP1 having four exons total - produce a stable, partially
    functional truncated protein that retains the N-terminal doublecortin (DCX)
    domain but loses distal sequence needed for normal regulation. This
    truncated product co-assembles with wild-type RP1 at the photoreceptor
    axoneme and interferes with normal microtubule/axoneme organization, a
    dominant-negative mechanism rather than simple haploinsufficiency. This is
    the more common RP1 disease mechanism and underlies the majority of
    RP1-related autosomal dominant RP.
  gene:
    preferred_term: RP1
    modifier: ABNORMAL
    term:
      id: hgnc:10263
      label: RP1
  genetic_context:
    gene:
      preferred_term: RP1
      term:
        id: hgnc:10263
        label: RP1
    functional_impact_category: DOMINANT_NEGATIVE
    description: >-
      Heterozygous middle-exon-4 truncating variants retain the BIF domain and
      produce an interfering truncated product rather than simply
      haploinsufficient loss of RP1 protein.
  cell_types:
  - preferred_term: retinal rod cell
    term:
      id: CL:0000604
      label: retinal rod cell
  - preferred_term: retinal cone cell
    term:
      id: CL:0000573
      label: retinal cone cell
  evidence:
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "the heterozygous variants will cause retinal degeneration with preserved BIF domain but loss of the unrecognized domain"
    explanation: >-
      Directly supports the dominant-negative model: heterozygous truncations
      that retain the BIF domain but lose additional distal sequence cause
      retinal degeneration despite the presence of one normal allele,
      consistent with an interfering truncated product rather than simple
      haploinsufficiency.
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "For the variants associated with adRP, the truncated production will preserve the BIF domain and may cause disease via a dominant-negative effect"
    explanation: >-
      Directly supports the dominant-negative (rather than haploinsufficient)
      mechanism for heterozygous RP1 truncating variants preserving the BIF
      domain.
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "the middle portion from c.1981 (p.661) to c.2749 (p.917)"
    explanation: >-
      Provides the precise coding-sequence/protein coordinates defining the
      middle-exon-4 region where heterozygous truncations act as
      dominant-negative alleles, refining the "middle portion" claim made by
      this node.
  downstream:
  - target: Photoreceptor Axoneme Disorganization
    description: >-
      The dominant-negative truncated protein disrupts normal RP1 function at
      the axoneme regardless of the co-expressed wild-type allele.

- name: Biallelic RP1 Loss
  description: >-
    Biallelic truncating variants located toward the N- or C-terminal ends of
    RP1 exon 4 (distinct from the middle-clustered dominant variants) produce
    complete loss of functional RP1 protein when present on both alleles.
    Heterozygous carriers of these same terminal variants are clinically
    unaffected, confirming that a single functional RP1 allele is sufficient
    for normal photoreceptor structure and that recessive disease requires
    complete loss rather than a dominant-negative product.
  gene:
    preferred_term: RP1
    modifier: ABSENT
    term:
      id: hgnc:10263
      label: RP1
  genetic_context:
    gene:
      preferred_term: RP1
      term:
        id: hgnc:10263
        label: RP1
    functional_impact_category: LOSS_OF_FUNCTION
    description: >-
      Biallelic N-/C-terminal truncating variants produce complete loss of
      functional RP1 protein; a single functional allele is sufficient for
      normal photoreceptor structure, so disease requires loss of both alleles.
  cell_types:
  - preferred_term: retinal rod cell
    term:
      id: CL:0000604
      label: retinal rod cell
  - preferred_term: retinal cone cell
    term:
      id: CL:0000573
      label: retinal cone cell
  evidence:
  - reference: PMID:32005865
    reference_title: "Retinitis Pigmentosa Due to Rp1 Biallelic Variants"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "They had classic retinitis pigmentosa with diagnosis at the first decade of life. The visual acuities were severely affected at a young age."
    explanation: >-
      Documents the severe, early-onset phenotype resulting from biallelic RP1
      loss-of-function variants, consistent with complete loss of RP1 function.
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Heterozygous truncations alone in the N- and C- terminals were unlikely pathogenic."
    explanation: >-
      A described negative control: this cohort's single heterozygous
      N-/C-terminal truncations were not enriched in RP patients and were
      judged unlikely pathogenic, directly supporting the claim that one
      functional RP1 allele is sufficient and that biallelic loss is required
      for recessive disease.
  downstream:
  - target: Photoreceptor Axoneme Disorganization
    description: >-
      Complete absence of functional RP1 protein disrupts axoneme organization
      more severely and from an earlier age than the dominant-negative
      mechanism.

- name: Photoreceptor Axoneme Disorganization
  description: >-
    RP1 is a photoreceptor-specific microtubule-associated protein located in
    the connecting cilium and axoneme, where it controls the length and
    stability of the axoneme and is required for correct orientation and
    higher-order stacking of outer segment discs. Loss of functional RP1 (via
    either the dominant-negative or recessive loss-of-function mechanism)
    disrupts this scaffolding role, producing misoriented, disorganized outer
    segment discs.
  cellular_components:
  - preferred_term: ciliary transition zone
    term:
      id: GO:0035869
      label: ciliary transition zone
  cell_types:
  - preferred_term: retinal rod cell
    term:
      id: CL:0000604
      label: retinal rod cell
  biological_processes:
  - preferred_term: cilium assembly
    modifier: ABNORMAL
    term:
      id: GO:0060271
      label: cilium assembly
  evidence:
  - reference: PMID:15269252
    reference_title: "The Retinitis Pigmentosa 1 Protein Is a Photoreceptor Microtubule-Associated Protein"
    supports: SUPPORT
    evidence_source: MODEL_ORGANISM
    snippet: "Disruption of the Rp1 gene in mice causes misorientation of outer segment discs, suggesting a role for RP1 in outer segment organization."
    explanation: >-
      Establishes RP1's structural role in outer segment disc organization
      using the Rp1 knockout mouse model; loss of RP1 causes disc
      misorientation, the direct structural consequence modeled by this node.
  - reference: PMID:15269252
    reference_title: "The Retinitis Pigmentosa 1 Protein Is a Photoreceptor Microtubule-Associated Protein"
    supports: SUPPORT
    evidence_source: MODEL_ORGANISM
    snippet: "we show that the RP1 protein is part of the photoreceptor axoneme"
    explanation: >-
      Establishes the subcellular localization of RP1 to the connecting
      cilium/axoneme, the structure disrupted in this node.
  downstream:
  - target: Rod Photoreceptor Apoptosis
    description: >-
      Disorganized, misoriented outer segment discs impair photoreceptor
      function and structural integrity over time, driving progressive rod
      photoreceptor degeneration.

- name: Rod Photoreceptor Apoptosis
  conforms_to: "photoreceptor_degeneration#Rod Photoreceptor Apoptosis"
  description: >-
    Progressive structural disorganization of the outer segment from
    dysfunctional RP1 ultimately drives rod photoreceptor apoptosis, the
    hallmark rod-predominant degeneration of retinitis pigmentosa producing
    nyctalopia and progressive peripheral visual field loss. Secondary cone
    degeneration follows as rods are lost. The recessive form progresses far
    more rapidly and with earlier macular involvement than the dominant form.
  cell_types:
  - preferred_term: retinal rod cell
    term:
      id: CL:0000604
      label: retinal rod cell
  biological_processes:
  - preferred_term: neuron apoptotic process
    modifier: INCREASED
    term:
      id: GO:0051402
      label: neuron apoptotic process
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
    explanation: >-
      Orphanet establishes progressive photoreceptor loss as the defining
      pathophysiological feature of retinitis pigmentosa, including RP1-RP.

phenotypes:
- category: Ophthalmologic
  name: Progressive Night Blindness
  frequency: VERY_FREQUENT
  description: >-
    Nyctalopia is the earliest and most common presenting symptom of RP1-related
    RP, reflecting rod-predominant photoreceptor dysfunction. Onset is generally
    earlier and more severe in recessive disease (reported cohort means in the
    early-to-mid teens) than in the comparatively milder, later-onset dominant
    form.
  phenotype_term:
    preferred_term: Progressive night blindness
    term:
      id: HP:0007675
      label: Progressive night blindness
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0007675 | Progressive night blindness | Very frequent (99-80%)"
    explanation: >-
      Orphanet records progressive night blindness as a very frequent feature
      of retinitis pigmentosa.
  - reference: PMID:20301590
    reference_title: "Nonsyndromic Retinitis Pigmentosa Overview."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Describe the clinical characteristics of nonsyndromic retinitis
      pigmentosa
    explanation: >-
      GeneReviews' clinical-characteristics scope for nonsyndromic RP,
      including RP1-related forms, covers presenting symptoms such as
      nyctalopia.

- category: Ophthalmologic
  name: Peripheral Visual Field Loss
  frequency: FREQUENT
  description: >-
    Progressive constriction of the visual field from the midperiphery inward
    as rod photoreceptors are lost, a cardinal feature of RP1-related RP.
  phenotype_term:
    preferred_term: Peripheral visual field loss
    term:
      id: HP:0007994
      label: Peripheral visual field loss
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0007994 | Peripheral visual field loss | Frequent (79-30%)"
    explanation: >-
      Orphanet records peripheral visual field loss as a frequent phenotype of
      retinitis pigmentosa.

- category: Ophthalmologic
  name: Bone Spicule Pigmentation of the Retina
  frequency: VERY_FREQUENT
  description: >-
    Characteristic mid-peripheral intraretinal pigment clumping on funduscopy,
    a hallmark sign of RP1-related RP as in other rod-cone dystrophies.
  phenotype_term:
    preferred_term: Bone spicule pigmentation of the retina
    term:
      id: HP:0007737
      label: Spicular pigmentation of the retina
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0007737 | Bone spicule pigmentation of the retina | Very frequent (99-80%)"
    explanation: >-
      Orphanet records bone spicule retinal pigmentation as a very frequent
      finding in retinitis pigmentosa.

- category: Ophthalmologic
  name: Attenuation of Retinal Blood Vessels
  frequency: FREQUENT
  description: >-
    Progressive retinal arteriolar narrowing, part of the classic RP fundus
    triad alongside bone spicule pigmentation and disc pallor.
  phenotype_term:
    preferred_term: Attenuation of retinal blood vessels
    term:
      id: HP:0007843
      label: Attenuation of retinal blood vessels
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0007843 | Attenuation of retinal blood vessels | Frequent (79-30%)"
    explanation: >-
      Orphanet records retinal vascular attenuation as a frequent feature of RP.

- category: Ophthalmologic
  name: Optic Disc Pallor
  frequency: FREQUENT
  description: >-
    Waxy pallor of the optic disc from nerve fiber layer loss, completing the
    classic RP funduscopic triad.
  phenotype_term:
    preferred_term: Optic disc pallor
    term:
      id: HP:0000543
      label: Optic disc pallor
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0000543 | Optic disc pallor | Frequent (79-30%)"
    explanation: >-
      Orphanet records optic disc pallor as a frequent finding in RP.

- category: Ophthalmologic
  name: Abnormal Electroretinogram
  frequency: VERY_FREQUENT
  description: >-
    Full-field ERG shows reduced-to-extinguished rod responses preceding cone
    involvement, the diagnostic cornerstone of RP1-related RP.
  phenotype_term:
    preferred_term: Abnormal electroretinogram
    term:
      id: HP:0000512
      label: Abnormal electroretinogram
  reports_on:
  - target: Photoreceptor Axoneme Disorganization
    relationship: READOUT_OF
    endpoint_context: DIAGNOSTIC
    interpretation: Full-field ERG measures rod (and later cone) photoreceptor function, which declines as axoneme/outer-segment disorganization progresses.
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0000512 | Abnormal electroretinogram | Very frequent (99-80%)"
    explanation: >-
      Orphanet records abnormal ERG as a very frequent finding in RP.

- category: Ophthalmologic
  name: Reduced Visual Acuity
  subtype: Recessive
  frequency: VERY_FREQUENT
  description: >-
    Recessive RP1-RP causes severe, early visual acuity loss, in contrast to
    the generally milder and later-onset acuity loss typical of dominant
    RP1-RP.
  phenotype_term:
    preferred_term: Reduced visual acuity
    term:
      id: HP:0007663
      label: Reduced visual acuity
  evidence:
  - reference: PMID:32005865
    reference_title: "Retinitis Pigmentosa Due to Rp1 Biallelic Variants"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "They had classic retinitis pigmentosa with diagnosis at the first decade of life. The visual acuities were severely affected at a young age."
    explanation: >-
      Documents the severe, early-onset visual acuity loss characteristic of
      recessive RP1-RP in a biallelic-variant cohort.
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "patients with arRP due to biallelic RP1 variants had a significantly earlier age at onset"
    explanation: >-
      Genotype-phenotype comparison in this pooled cohort found significantly
      earlier age at onset for biallelic (recessive) RP1 patients than for
      heterozygous (dominant) RP1 patients, a quantified statistic supporting
      the earlier/more-severe recessive course modeled by this node.

- category: Ophthalmologic
  name: Macular Atrophy
  subtype: Recessive
  frequency: VERY_FREQUENT
  description: >-
    Macular atrophy, with secondary macular involvement, is a common to
    near-universal finding in biallelic (recessive) RP1-RP cohorts, and
    contributes to the more severe visual outcome of the recessive form
    relative to dominant disease.
  phenotype_term:
    preferred_term: Macular atrophy
    term:
      id: HP:0007401
      label: Macular atrophy
  evidence:
  - reference: PMID:32565670
    reference_title: "Biallelic RP1-associated retinal dystrophies: Expanding the mutational and clinical spectrum"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Macular atrophy was a common feature across the cohort."
    explanation: >-
      Directly reports macular atrophy as a common feature (FREQUENT band)
      across this biallelic RP1 cohort.
  - reference: PMID:32005865
    reference_title: "Retinitis Pigmentosa Due to Rp1 Biallelic Variants"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Macular atrophy was found in almost all patients"
    explanation: >-
      Reports macular atrophy in almost all patients of this biallelic RP1
      cohort, mapping to the VERY_FREQUENT band under the DisMech qualitative
      frequency mapping.

- category: Ophthalmologic
  name: Progressive Visual Loss
  frequency: VERY_FREQUENT
  description: >-
    Progressive loss of vision over decades is the natural history of RP1-RP in
    both inheritance forms, though the recessive form progresses faster and
    from an earlier baseline than the generally milder, later-onset dominant
    form.
  phenotype_term:
    preferred_term: Progressive visual loss
    term:
      id: HP:0000529
      label: Progressive visual loss
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
    explanation: >-
      Orphanet establishes progressive photoreceptor loss over decades as the
      defining natural history of retinitis pigmentosa, including RP1-RP.

genetic:
- name: RP1 pathogenic variants
  gene_term:
    preferred_term: RP1
    term:
      id: hgnc:10263
      label: RP1
  association: Causative
  features: >-
    Nearly all known pathogenic variants are nonsense or frameshift changes
    clustered in RP1's coding exons, predominantly exon 4 (which alone encodes
    more than 85% of the 2,156-amino-acid protein despite RP1 having four exons
    total), predicted to truncate the protein by approximately 50-70%. Variants
    located in the middle portion of exon 4 act as heterozygous dominant-negative alleles
    causing autosomal dominant RP; variants toward the N- or C-terminal ends of
    exon 4 require biallelic inheritance to cause the generally more severe
    autosomal recessive form (with exon-2 missense variants forming a
    later-onset exception). Studies have excluded simple haploinsufficiency as
    the causative mechanism for the dominant form.
  inheritance:
  - name: Autosomal dominant
    evidence:
    - reference: PMID:33681214
      reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "truncations in the middle portion are associated with adRP, while those in the N- and C- terminals are responsible for arRP, which was supported by most truncation variants (91.9%, 147/160)"
      explanation: >-
        Confirms that RP1 truncating-variant position (middle exon 4 vs.
        N-/C-terminal) predicts inheritance pattern (dominant vs. recessive)
        in 91.9% (147/160) of reported truncations, the positional rule
        underlying this entry's dominant-negative-versus-loss-of-function
        model.
  - name: Autosomal recessive
    evidence:
    - reference: PMID:32005865
      reference_title: "Retinitis Pigmentosa Due to Rp1 Biallelic Variants"
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "They had classic retinitis pigmentosa with diagnosis at the first decade of life. The visual acuities were severely affected at a young age."
      explanation: >-
        Documents a cohort of patients with biallelic RP1 variants presenting
        with early-onset autosomal recessive RP.
  evidence:
  - reference: PMID:15269252
    reference_title: "The Retinitis Pigmentosa 1 Protein Is a Photoreceptor Microtubule-Associated Protein"
    supports: SUPPORT
    evidence_source: MODEL_ORGANISM
    snippet: "RP1 is a MAP. Given the specific expression of RP1 in photoreceptors, RP1 is thus the first photoreceptor-specific MAP to be identified."
    explanation: >-
      Establishes RP1 as a photoreceptor-specific microtubule-associated
      protein, the functional basis for its role in RP.

diagnosis:
- name: Full-Field Electroretinography (ERG)
  description: >-
    Full-field ERG is the diagnostic cornerstone for RP1-related RP, showing a
    rod-cone pattern of dysfunction that is milder and later-onset in dominant
    disease than in recessive disease.
  diagnosis_term:
    preferred_term: electroretinogram procedure
    term:
      id: NCIT:C101217
      label: Retinal Examination
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "HP:0000512 | Abnormal electroretinogram | Very frequent (99-80%)"
    explanation: >-
      The very high frequency of abnormal ERG in RP supports ffERG as a core
      diagnostic investigation for RP1-RP.

- name: Molecular Genetic Testing
  description: >-
    Sequencing of RP1's coding exons - particularly exon 4, which alone encodes
    more than 85% of the protein and harbors most known pathogenic variants -
    identifies the truncating variants responsible for both dominant and
    recessive disease. Variant position within exon 4 (middle vs. terminal) and
    zygosity together determine expected inheritance pattern and prognosis,
    informing genetic counseling.
  diagnosis_term:
    preferred_term: genetic testing
    term:
      id: NCIT:C15709
      label: Genetic Testing
  evidence:
  - reference: PMID:33681214
    reference_title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "RP1 is listed as the top seventh of the most frequently implicated genes in inherited retinal disease based on a large cohort."
    explanation: >-
      Supports the clinical value of including RP1 in molecular genetic
      testing panels for inherited retinal disease given its high frequency.
  - reference: PMID:20301590
    reference_title: "Nonsyndromic Retinitis Pigmentosa Overview."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Provide an evaluation strategy to identify the genetic cause of
      nonsyndromic retinitis pigmentosa in a proband
    explanation: >-
      GeneReviews frames molecular genetic testing as the evaluation strategy
      for identifying the genetic cause of nonsyndromic RP, including RP1.

treatments:
- name: Low Vision Rehabilitation
  therapeutic_modality: OTHER
  description: >-
    Low vision aids, orientation and mobility training, and adaptive technology
    are the mainstay of management for RP1-related RP, particularly important
    for the early and severe visual loss of recessive disease.
  treatment_term:
    preferred_term: supportive care
    term:
      id: NCIT:C15747
      label: Supportive Care
  target_phenotypes:
  - preferred_term: Progressive visual loss
    term:
      id: HP:0000529
      label: Progressive visual loss
  evidence:
  - reference: "ORPHA:791"
    reference_title: "Retinitis pigmentosa"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Retinitis pigmentosa (RP) is an inherited retinal dystrophy leading to progressive loss of the photoreceptors and retinal pigment epithelium and resulting in blindness usually after several decades."
    explanation: >-
      Progressive visual impairment in RP justifies ongoing low-vision
      rehabilitation as the primary symptomatic management strategy.
  - reference: PMID:20301590
    reference_title: "Nonsyndromic Retinitis Pigmentosa Overview."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Provide a brief summary of management of nonsyndromic retinitis
      pigmentosa
    explanation: >-
      GeneReviews includes a management summary for nonsyndromic RP,
      including RP1-related forms, of which low vision rehabilitation is a
      core component.

- name: Genetic Counseling
  therapeutic_modality: OTHER
  description: >-
    Essential given RP1's unusual dual inheritance pattern: counseling must
    distinguish the 50% recurrence risk and generally milder course of
    dominant disease from the 25% recurrence risk and generally more severe
    course of recessive disease, which depend on where in exon 4 (and, for
    biallelic variants, whether an exon-2 missense allele is involved) the
    family's variant(s) fall.
  treatment_term:
    preferred_term: Genetic Counseling
    term:
      id: NCIT:C15240
      label: Genetic Counseling
  evidence:
  - reference: PMID:22317909
    reference_title: "RP1 and retinitis pigmentosa: report of novel mutations and insight into mutational mechanism"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "RP1 is one of the earliest identified disease genes in RP with mutations in this gene known to act both recessively and dominantly although the mutational mechanism remains unclear."
    explanation: >-
      RP1's dual inheritance pattern, with mechanism-dependent recurrence risk,
      underscores the need for genotype-specific genetic counseling.
  - reference: PMID:20301590
    reference_title: "Nonsyndromic Retinitis Pigmentosa Overview."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Inform genetic risk assessment of family members of a proband with
      nonsyndromic retinitis pigmentosa
    explanation: >-
      GeneReviews explicitly scopes this overview to inform genetic risk
      assessment of family members, the core purpose of genetic counseling
      modeled by this node.

references:
- reference: PMID:15269252
  title: "The Retinitis Pigmentosa 1 Protein Is a Photoreceptor Microtubule-Associated Protein"
- reference: PMID:33681214
  title: "Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions"
- reference: PMID:22317909
  title: "RP1 and retinitis pigmentosa: report of novel mutations and insight into mutational mechanism"
- reference: PMID:32005865
  title: "Retinitis Pigmentosa Due to Rp1 Biallelic Variants"
- reference: PMID:32565670
  title: "Biallelic RP1-associated retinal dystrophies: Expanding the mutational and clinical spectrum"
- reference: PMID:20664799
  title: "Differential pattern of RP1 mutations in retinitis pigmentosa."
- reference: PMID:20301590
  title: "Nonsyndromic Retinitis Pigmentosa Overview."
  tags:
  - GeneReviews
- reference: "ORPHA:791"
  title: "Retinitis pigmentosa"
📚

References & Deep Research

References

8
The Retinitis Pigmentosa 1 Protein Is a Photoreceptor Microtubule-Associated Protein
No top-level findings curated for this source.
Dominant RP in the Middle While Recessive in Both the N- and C-Terminals Due to RP1 Truncations: Confirmation, Refinement, and Questions
No top-level findings curated for this source.
RP1 and retinitis pigmentosa: report of novel mutations and insight into mutational mechanism
No top-level findings curated for this source.
Retinitis Pigmentosa Due to Rp1 Biallelic Variants
No top-level findings curated for this source.
Biallelic RP1-associated retinal dystrophies: Expanding the mutational and clinical spectrum
No top-level findings curated for this source.
Differential pattern of RP1 mutations in retinitis pigmentosa.
No top-level findings curated for this source.
Nonsyndromic Retinitis Pigmentosa Overview.
No top-level findings curated for this source.
Retinitis pigmentosa
No top-level findings curated for this source.