MTFR1L

Chr 1

mitochondrial fission regulator 1 like

Also known as: FAM54B, HYST1888, MST116, MSTP116

MTFR1L encodes a mitochondrial protein that regulates mitochondrial morphology and mediates stress-induced mitochondrial fragmentation by controlling OPA1 levels in response to metabolic changes. Mutations cause autosomal recessive developmental and epileptic encephalopathy with microcephaly and brain atrophy, typically presenting in infancy. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.61), and the disorder primarily affects the central nervous system with severe neurodevelopmental impairment.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.61
Clinical SummaryMTFR1L
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.24) despite low pLI — interpret in context.
📋
ClinVar Variants
5 unique Pathogenic / Likely Pathogenic· 42 VUS of 60 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.61LOEUF
pLI 0.313
Z-score 2.52
OE 0.24 (0.110.61)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.05Z-score
OE missense 0.77 (0.670.89)
128 obs / 166.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.24 (0.110.61)
00.351.4
Missense OE0.77 (0.670.89)
00.61.4
Synonymous OE1.16
01.21.6
LoF obs/exp: 3 / 12.7Missense obs/exp: 128 / 166.0Syn Z: -1.00
DN
0.6745th %ile
GOF
0.6930th %ile
LOF
0.4529th %ile

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

GOFprediction above median
DNprediction 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

60 submitted variants in ClinVar

Classification Summary

Pathogenic5
VUS42
Likely Benign5
5
Pathogenic
42
VUS
5
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
5
0
5
Likely Pathogenic
0
0
0
0
0
VUS
0
36
6
0
42
Likely Benign
1
3
0
1
5
Benign
0
0
0
0
0
Total13911152

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

View in ClinVar →

Protein Context — Lollipop Plot

MTFR1L · 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 →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC