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IEMbase 0739: ATP5F1A-related mitochondrial ATP synthase F1 alpha deficiency

Scope

Field Value
IEMbase ID 739
Nosology 7.5.01.02
Nosology code IEM0481
Gene ATP5F1A
External IDs OMIM:616045; OMIM:615228; ORPHA:254913
Generated mapping CANDIDATE; fuzzy SCO1-Related_COX_Deficiency.yaml
Candidate DisMech targets Broad complex V context only; no exact ATP5F1A target identified
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents autosomal recessive ATP5F1A-related mitochondrial ATP synthase F1 subunit alpha deficiency, with alternate labels combined oxidative phosphorylation deficiency 22 and mitochondrial complex V deficiency, nuclear type 4. The cached rows are sparse but neonatal/infantile: increased plasma alanine, asymmetric white matter lesions, irritability, neonatal nystagmus, infantile perinatal death, neonatal/infantile hypotonia, and neonatal/infantile microcephaly.

DisMech phenotype coverage

No exact ATP5F1A target was identified locally.

The generated SCO1-Related_COX_Deficiency.yaml candidate is a false positive. SCO1 is a nuclear complex IV copper-delivery disorder with hepatic failure, encephalopathy, lactic acidosis, seizures, and hypopituitarism; it is not an ATP synthase F1 alpha subunit disease. NARP_syndrome.yaml and Myopathy_Lactic_Acidosis_and_Sideroblastic_Anemia.yaml are useful complex V context, but they are MT-ATP6/8 or syndrome-specific and do not model ATP5F1A.

Concordance and completeness

Judgement: true ATP5F1A complex V local gap. Reject the SCO1 candidate as exact coverage.

IEMbase supplies a concise neonatal phenotype seed: alanine elevation, white matter lesions, irritability, nystagmus, hypotonia, microcephaly, and early death. DisMech currently has no ATP5F1A-specific structural ATP synthase entry.

Curation actions

  • Add ATP5F1A-related mitochondrial complex V deficiency / COXPD22 to the complex V backlog.
  • Reject SCO1-Related_COX_Deficiency.yaml as exact coverage.
  • Preserve alanine, asymmetric white matter lesions, irritability, nystagmus, hypotonia, microcephaly, and perinatal-death prompts.