PHC1

Chr 12AR

polyhomeotic homolog 1

Also known as: EDR1, HPH1, MCPH11, RAE28

The protein is a component of the Polycomb repressive complex that regulates gene expression through chromatin modification and contains conserved domains that mediate protein-protein interactions with other Polycomb group proteins. Loss-of-function mutations cause primary microcephaly 11, an autosomal recessive disorder characterized by reduced brain size. The high pLI score indicates this gene is highly intolerant to loss-of-function variants, consistent with haploinsufficiency being pathogenic.

OMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismARLOEUF 0.241 OMIM phenotype
Clinical SummaryPHC1
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
38 unique Pathogenic / Likely Pathogenic· 148 VUS of 241 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.24LOEUF
pLI 0.999
Z-score 5.40
OE 0.12 (0.060.24)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
1.92Z-score
OE missense 0.76 (0.690.82)
375 obs / 495.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.12 (0.060.24)
00.351.4
Missense OE0.76 (0.690.82)
00.61.4
Synonymous OE1.01
01.21.6
LoF obs/exp: 5 / 43.3Missense obs/exp: 375 / 495.1Syn Z: -0.12
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedPHC1-related primary microcephalyOTHERAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.2897th %ile
GOF
0.2796th %ile
LOF
0.80top 5%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

241 submitted variants in ClinVar

Classification Summary

Pathogenic35
Likely Pathogenic3
VUS148
Likely Benign18
Benign27
35
Pathogenic
3
Likely Pathogenic
148
VUS
18
Likely Benign
27
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
34
0
35
Likely Pathogenic
0
1
2
0
3
VUS
0
141
6
1
148
Likely Benign
1
4
2
11
18
Benign
0
4
19
4
27
Total21506316231

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

PHC1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC