The protein functions as a mitochondrial outer membrane protein that mediates mitochondrial fusion and maintains the mitochondrial network. Mutations cause autosomal dominant and autosomal recessive forms of Charcot-Marie-Tooth disease type 2A2 and hereditary motor and sensory neuropathy VI, both axonal peripheral neuropathies, as well as multiple symmetric lipomatosis. The high pLI score (0.99) and low LOEUF score (0.28) indicate the gene is highly intolerant to loss-of-function variants, suggesting pathogenicity occurs through haploinsufficiency or dominant-negative mechanisms.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAD/ARLOEUF 0.284 OMIM phenotypes
Clinical SummaryMFN2
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Gene-Disease Validity (ClinGen)
obsolete axonal hereditary motor and sensory neuropathy · SDDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.28LOEUF
pLI 0.994
Z-score 4.90
OE 0.13 (0.070.28)
Highly constrained

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

Missense Constraint
1.66Z-score
OE missense 0.77 (0.700.85)
326 obs / 421.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.13 (0.070.28)
00.351.4
Missense OE0.77 (0.700.85)
00.61.4
Synonymous OE1.05
01.21.6
LoF obs/exp: 5 / 37.3Missense obs/exp: 326 / 421.8Syn Z: -0.53
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateMFN2-related developmental disorderOTHERAD
definitiveMFN2-related Charcot-Marie-Tooth disease, axonalOTHERAR
definitiveMFN2-related hereditary motor and sensory neuropathyOTHERAD
DN
0.5181th %ile
GOF
0.5269th %ile
LOF
0.59top 25%

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

LOFLOEUF 0.28
GOF1 literature citation
DN1 literature citation

Literature Evidence

DNWhile mitochondrial aggregates were labeled for mitophagy, mutant MFN2 did not inhibit Parkin-mediated degradation, but instead had a dominant negative effect on mitochondrial fusion only when MFN1 was at low levels, as occurs in neurons.PMID:30882371
GOFPich et al. (2005) showed that Mfn2 loss of function inhibited pyruvate, glucose, and fatty acid oxidation and reduced mitochondrial membrane potential, whereas Mfn2 gain of function increased glucose oxidation and mitochondrial membrane potential.PMID:15829499

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

MFN2 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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