PRDM5

Chr 4AR

PR/SET domain 5

Also known as: BCS2, PFM2

PRDM5 encodes a transcription factor that represses gene expression through recruitment of histone methyltransferases and deacetylases, and regulates expression of extracellular matrix proteins including fibrillar collagens. Mutations cause brittle cornea syndrome 2, an autosomal recessive connective tissue disorder characterized by fragile corneas and associated ocular abnormalities. The gene shows very low constraint against loss-of-function variants (pLI near zero), consistent with its recessive inheritance pattern.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Brittle cornea syndrome 2MIM #614170
AR
0
Active trials
4
Pubs (1 yr)
54
P/LP submissions
5%
P/LP missense
0.84
LOEUF
LOF
Mechanism· G2P
Clinical SummaryPRDM5
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
43 unique Pathogenic / Likely Pathogenic· 184 VUS of 600 total submissions
📖
GeneReview available — PRDM5
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.84LOEUF
pLI 0.000
Z-score 2.32
OE 0.58 (0.410.84)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.70Z-score
OE missense 0.89 (0.810.98)
305 obs / 341.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.58 (0.410.84)
00.351.4
Missense OE0.89 (0.810.98)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 21 / 36.1Missense obs/exp: 305 / 341.3Syn Z: -1.29
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedPRDM5-related Axenfeld-Rieger syndromeOTHERAD
definitivePRDM5-related Brittle cornea syndromeLOFAR
DN
0.6841th %ile
GOF
0.6345th %ile
LOF
0.3551th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

600 submitted variants in ClinVar

Classification Summary

Pathogenic24
Likely Pathogenic19
VUS184
Likely Benign293
Benign46
Conflicting25
24
Pathogenic
19
Likely Pathogenic
184
VUS
293
Likely Benign
46
Benign
25
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
7
0
17
0
24
Likely Pathogenic
13
2
4
0
19
VUS
2
170
12
0
184
Likely Benign
1
14
148
130
293
Benign
0
0
46
0
46
Conflicting
25
Total23186227130591

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

View in ClinVar →

Protein Context — Lollipop Plot

PRDM5 · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →