Activity

Filter

Cancel
Date Panel Item Activity
10 actions
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska changed review comment from: PMID: 41895291 Lambton et al, 2026
Homozygous and compound heterozygous variants in ATG12 reported in 6 individuals from five unrelated families with neurodevelopmental disorder with hypotonia, seizures (all 6 individuals with variable severity), ataxia, developmental delay and / or intellectual disability (seen in all 5 families), corpus callosum hypoplasia (4/5 individuals) and hypoplasia of the cerebellar vermis (5/5 individuals assessed). Other less consistent MRI findings: reduced white and gray matter, polymicrogyria, cerebellocerebral atrophy, thinning of pons, brainstem hypomyelination, and more. 4/6 individuals died before age 5 years.

Family 1: 2 sibs with ATG12 variants c.359A>C, p.Tyr120Ser and c.363+3A>T (demonstrated to cause exon 3 skipping)
Family 2: proband with a homozygous variant c.413C>T, p.Ala138Val
Family 3 : proband with a homozygous variant c.359A>C p.Tyr.120Ser
Family 4: proband S5 comp het for ATG12 variants c.235C>T (p.Arg79∗) & c.359A>C p.Tyr.120Ser
Family 5: proabdn with homozygous missense variant c.324T>G (p.Phe108Leu)

Functional: Loss of atg12 function in zebrafish causes developmental delay, impaired brain function, and pre-adult lethality.

This gene has no disease association in OMIM (accessed 1st Apr 2026).
Sources: Literature; to: PMID: 41895291 Lambton et al, 2026
Homozygous and compound heterozygous variants in ATG12 reported in 6 individuals from five unrelated families with neurodevelopmental disorder with hypotonia, seizures (all 6 individuals with variable severity), ataxia, developmental delay and / or intellectual disability (seen in all 5 families), corpus callosum hypoplasia (4/5 individuals) and hypoplasia of the cerebellar vermis (5/5 individuals assessed). Other less consistent MRI findings: reduced white and gray matter, polymicrogyria, cerebellocerebral atrophy, thinning of pons, brainstem hypomyelination, and more. 4/6 individuals died before age 5 years.

Family 1: 2 sibs with ATG12 variants c.359A>C, p.Tyr120Ser and c.363+3A>T (demonstrated to cause exon 3 skipping)
Family 2: proband with a homozygous variant c.413C>T, p.Ala138Val
Family 3 : proband with a homozygous variant c.359A>C p.Tyr.120Ser
Family 4: proband S5 comp het for ATG12 variants c.235C>T (p.Arg79∗) & c.359A>C p.Tyr.120Ser
Family 5: proband with homozygous missense variant c.324T>G (p.Phe108Leu)

Functional: Loss of atg12 function in zebrafish causes developmental delay, impaired brain function, and pre-adult lethality.

This gene has no disease association in OMIM (accessed 1st Apr 2026).
Sources: Literature
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska changed review comment from: PMID: 41895291 Lambton et al, 2026
Homozygous and compound heterozygous variants in ATG12 reported in 6 individuals from five unrelated families with neurodevelopmental disorder with hypotonia, seizures (all 6 individuals with variable severity), ataxia, developmental delay and / or intellectual disability (seen in all 5 families), corpus callosum hypoplasia (4/5 individuals) and hypoplasia of the cerebellar vermis (5/5 individuals assessed). Other less consistent MRI findings: reduced white and gray matter, polymicrogyria, cerebellocerebral atrophy, thinning of pons, brainstem hypomyelination, and more. 4/6 individuals died before age 5 years.

Family 1: 2 sibs with ATG12 variants c.359A>C, p.Tyr120Ser and c.363+3A>T (demonstrated to cause exon 3 skipping)
Family 2: proband with a homozygous variant c.413C>T, p.Ala138Val
Family 3 : proband with a homozygous variant c.359A>C p.Tyr.120Ser
Family 4: proband S5 comp het for ATG12 variants c.235C>T (p.Arg79∗) & c.359A>C p.Tyr.120Ser
Family 5: proabdn with homozygous missense variant c.324T>G (p.Phe108Leu)

This gene has no disease association in OMIM (accessed 1st Apr 2026).
Sources: Literature; to: PMID: 41895291 Lambton et al, 2026
Homozygous and compound heterozygous variants in ATG12 reported in 6 individuals from five unrelated families with neurodevelopmental disorder with hypotonia, seizures (all 6 individuals with variable severity), ataxia, developmental delay and / or intellectual disability (seen in all 5 families), corpus callosum hypoplasia (4/5 individuals) and hypoplasia of the cerebellar vermis (5/5 individuals assessed). Other less consistent MRI findings: reduced white and gray matter, polymicrogyria, cerebellocerebral atrophy, thinning of pons, brainstem hypomyelination, and more. 4/6 individuals died before age 5 years.

Family 1: 2 sibs with ATG12 variants c.359A>C, p.Tyr120Ser and c.363+3A>T (demonstrated to cause exon 3 skipping)
Family 2: proband with a homozygous variant c.413C>T, p.Ala138Val
Family 3 : proband with a homozygous variant c.359A>C p.Tyr.120Ser
Family 4: proband S5 comp het for ATG12 variants c.235C>T (p.Arg79∗) & c.359A>C p.Tyr.120Ser
Family 5: proabdn with homozygous missense variant c.324T>G (p.Phe108Leu)

Functional: Loss of atg12 function in zebrafish causes developmental delay, impaired brain function, and pre-adult lethality.

This gene has no disease association in OMIM (accessed 1st Apr 2026).
Sources: Literature
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska changed review comment from: Comment on list classification: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient (walking with support at 17yo), with 2 other cases that were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.; to: Comment on list classification: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient (walking with support at 17yo), while 2 other individuals were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska changed review comment from: Comment on list classification: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient, with 2 other cases that were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.; to: Comment on list classification: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient (walking with support at 17yo), with 2 other cases that were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska Classified gene: ATG12 as Amber List (moderate evidence)
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska Added comment: Comment on list classification: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient, with 2 other cases that were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.
Ataxia and cerebellar anomalies - narrow panel v8.74 ATG12 Ida Ertmanska Gene: atg12 has been classified as Amber List (Moderate Evidence).
Ataxia and cerebellar anomalies - narrow panel v8.73 ATG12 Ida Ertmanska Deleted their comment
Ataxia and cerebellar anomalies - narrow panel v8.73 ATG12 Ida Ertmanska commented on gene: ATG12: There are 5 unrelated families reported in literature with individuals harbouring biallelic ATG12 variants and presenting with hypoplasia of the cerebellar vermis on MRI. Ataxia was diagnosed in 1 patient, with 2 other cases that were nonambulant. Based on available evidence, this gene should be promoted to Green on Ataxia and cerebellar anomalies - narrow panel.
Ataxia and cerebellar anomalies - narrow panel v8.73 ATG12 Ida Ertmanska gene: ATG12 was added
gene: ATG12 was added to Ataxia and cerebellar anomalies - narrow panel. Sources: Literature
Q2_26_promote_green tags were added to gene: ATG12.
Mode of inheritance for gene: ATG12 was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: ATG12 were set to 41895291
Phenotypes for gene: ATG12 were set to neurodevelopmental disorder, MONDO:0700092; Hypoplasia of the corpus callosum, HP:0002079; Cerebellar hypoplasia, HP:0001321
Review for gene: ATG12 was set to GREEN
Added comment: PMID: 41895291 Lambton et al, 2026
Homozygous and compound heterozygous variants in ATG12 reported in 6 individuals from five unrelated families with neurodevelopmental disorder with hypotonia, seizures (all 6 individuals with variable severity), ataxia, developmental delay and / or intellectual disability (seen in all 5 families), corpus callosum hypoplasia (4/5 individuals) and hypoplasia of the cerebellar vermis (5/5 individuals assessed). Other less consistent MRI findings: reduced white and gray matter, polymicrogyria, cerebellocerebral atrophy, thinning of pons, brainstem hypomyelination, and more. 4/6 individuals died before age 5 years.

Family 1: 2 sibs with ATG12 variants c.359A>C, p.Tyr120Ser and c.363+3A>T (demonstrated to cause exon 3 skipping)
Family 2: proband with a homozygous variant c.413C>T, p.Ala138Val
Family 3 : proband with a homozygous variant c.359A>C p.Tyr.120Ser
Family 4: proband S5 comp het for ATG12 variants c.235C>T (p.Arg79∗) & c.359A>C p.Tyr.120Ser
Family 5: proabdn with homozygous missense variant c.324T>G (p.Phe108Leu)

This gene has no disease association in OMIM (accessed 1st Apr 2026).
Sources: Literature