SPTLC1

Chr 9AD

serine palmitoyltransferase long chain base subunit 1

Also known as: ALS27, HSAN1, HSN1, LBC1, LCB1, SPT1, SPTI

The protein is the long chain base subunit 1 of serine palmitoyltransferase, which catalyzes the initial and rate-limiting step in sphingolipid biosynthesis by condensing L-serine with activated acyl-CoA. Mutations cause hereditary sensory and autonomic neuropathy type IA and juvenile amyotrophic lateral sclerosis, both inherited in an autosomal dominant pattern. The gene shows very low constraint against loss-of-function variants (pLI near 0), suggesting the pathogenic variants likely affect protein function through other mechanisms.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.982 OMIM phenotypes
Clinical SummarySPTLC1
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Gene-Disease Validity (ClinGen)
neuropathy, hereditary sensory and autonomic, type 1A · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.98LOEUF
pLI 0.000
Z-score 1.65
OE 0.68 (0.480.98)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.13Z-score
OE missense 0.80 (0.720.90)
208 obs / 259.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.68 (0.480.98)
00.351.4
Missense OE0.80 (0.720.90)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 21 / 30.9Missense obs/exp: 208 / 259.2Syn Z: -0.30
DN
0.6550th %ile
GOF
0.5269th %ile
LOF
0.3453th %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 · 1 literature citation
GOF1 literature citation

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

DNThese results indicate that the HSN1-associated mutations in LCB1 confer dominant negative effects on the SPT enzyme.PMID:12417569
GOFThis observation is consistent with the hypothesis that HSAN1 is the result of a gain-of-function mutation in SPTLC1 that leads to accumulation of a toxic metabolite.PMID:19923297

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

SPTLC1 · 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.

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Clinical Literature
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