PTDSS1

Chr 8AD

phosphatidylserine synthase 1

Also known as: LMHD, PSS1, PSSA

This enzyme catalyzes the formation of phosphatidylserine from phosphatidylcholine or phosphatidylethanolamine through a base-exchange reaction, producing a critical membrane phospholipid involved in cellular structure and signaling. Mutations cause Lenz-Majewski hyperostotic dwarfism, a rare disorder characterized by skeletal abnormalities and overgrowth, with autosomal dominant inheritance. The gene is highly constrained against loss-of-function variants (LOEUF 0.448), indicating it is intolerant to complete protein loss.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Lenz-Majewski hyperostotic dwarfismMIM #151050
AD
0
Active trials
14
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.45
LOEUF
GOF
Mechanism· G2P
Clinical SummaryPTDSS1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.25) despite low pLI — interpret in context.
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GeneReview available — PTDSS1
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.45LOEUF
pLI 0.151
Z-score 3.95
OE 0.25 (0.140.45)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.38Z-score
OE missense 0.59 (0.520.67)
158 obs / 267.4 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.25 (0.140.45)
00.351.4
Missense OE0.59 (0.520.67)
00.61.4
Synonymous OE0.94
01.21.6
LoF obs/exp: 8 / 32.2Missense obs/exp: 158 / 267.4Syn Z: 0.47
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitivePTDSS1-related Lenz-Majewski hyperostotic dwarfismGOFAD
limitedPTDSS1-related developmental delayOTHERAD
DN
0.6744th %ile
GOF
0.6736th %ile
LOF
0.3551th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function, dominant-negative and loss-of-function). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median · 1 literature citation
DNprediction above median
LOF1 literature citation · LOEUF 0.45

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.

Literature Evidence

GOFGain-of-function mutations in the phosphatidylserine synthase 1 (PTDSS1) gene cause Lenz-Majewski syndrome.PMID:24241535
LOFThis is the first report of the clinical phenotype seen in an individual with a heterozygous loss-of-function variant in PTDSS1.PMID:35224839

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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

PTDSS1 · 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.

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Clinical Literature
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Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗