rs387906420

Variant summary

Our verdict is Likely pathogenic. The variant received 6 ACMG points: 6P and 0B. PS4_ModeratePP1_ModeratePP3PM2_Supporting

This summary comes from the ClinGen Evidence Repository: The m.616T>C variant in MT-TF has been reported in at least 12 individuals from six families with features of a primary mitochondrial disease. Affected individuals had variable ages of onset (first few months of life with delays or seizures at 10 months old to late teenage years with renal disease or epilepsy). Several individuals had chronic kidney disease or renal failure; some even had transplants with non-recurrence of disease post-transplant. Other symptoms reported include developmental delay, epilepsy, status epilepticus (EPC), and myoclonus. Muscle biopsy revealed COX negative fibers. Heteroplasmy levels were the same in all affected probands as the variant was present at homoplasmy or > 97% in all tissues. Of note, some healthy family members had the variant at lower heteroplasmy levels but in at least one healthy family member, the variant was present at a heteroplasmy level as high as 92% (PS4_moderate; PMIDs: 31722346, 28267784, 20142618). There are no reports of de novo occurrence of this variant. This variant segregated with disease in multiple affected members in multiple families and several healthy family members had lower or undetectable levels of the variant (PP1_moderate; PMIDs: 31722346, 28267784, 20142618). This variant is absent in the GenBank dataset, Helix dataset, and gnomAD v3.1.2 (PM2_supporting). There is one cybrid study for this variant however the cybrid also had another mtDNA variant precluding scoring for PS3. There are no single fiber studies or other functional assays reported for this variant. The computational predictor MitoTIP suggests this variant is pathogenic (83.3 percentile) and HmtVAR predicts it to be pathogenic score of 0.5 (PP3). In summary, this variant meets criteria to be classified as likely pathogenic for primary mitochondrial disease inherited in a mitochondrial manner. This classification was approved by the NICHD/NINDS U24 Mitochondrial Disease Variant Curation Expert Panel on June 13, 2022. Mitochondrial DNA-specific ACMG/AMP criteria applied (PMID:32906214): PS4_moderate, PP1_moderate, PP3, PM2_supporting. LINK:https://erepo.genome.network/evrepo/ui/classification/CA120552/MONDO:0044970/014

Frequency

Mitomap GenBank:
Absent

Consequence

TRNF
unassigned_transcript_4784 missense

Scores

Mitotip
Pathogenic
17

Clinical Significance

Likely pathogenic reviewed by expert panel P:5
Maternally-inherited-epilepsy-/-mito-tubulointerstitial-kidney-disease-(MITKD)-/-Gitelman-like-syndrome,Maternally-inherited-epilepsy

Conservation

PhyloP100: 3.71

Publications

1 publications found
Variant links:
Genes affected
TRNF (HGNC:7481): (mitochondrially encoded tRNA phenylalanine)
MT-RNR1 (HGNC:7470): (mitochondrially encoded 12S RNA) Enables DNA binding activity and DNA-binding transcription factor binding activity. Involved in several processes, including osteoblast proliferation; regulation of carbohydrate utilization; and regulation of phosphate metabolic process. Located in extracellular space; mitochondrion; and nucleus. [provided by Alliance of Genome Resources, Apr 2022]
MT-RNR1 Gene-Disease associations (from GenCC):
  • mitochondrial disease
    Inheritance: Mitochondrial Classification: DEFINITIVE Submitted by: ClinGen

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ACMG classification

Classification was made for transcript

Our verdict: Likely_pathogenic. The variant received 6 ACMG points.

PS4
For more information check the summary or visit ClinGen Evidence Repository.
PM2
For more information check the summary or visit ClinGen Evidence Repository.
PP1
For more information check the summary or visit ClinGen Evidence Repository.
PP3
For more information check the summary or visit ClinGen Evidence Repository.

Transcripts

RefSeq

Gene Transcript HGVSc HGVSp Effect Exon rank MANE Protein UniProt
TRNFunassigned_transcript_4784 c.40T>C p.Cys14Arg missense_variant Exon 1 of 1
RNR1unassigned_transcript_4785 n.-32T>C upstream_gene_variant

Ensembl

Gene Transcript HGVSc HGVSp Effect Exon rank TSL MANE Protein Appris UniProt
MT-TFENST00000387314.1 linkn.40T>C non_coding_transcript_exon_variant Exon 1 of 1 6
MT-RNR1ENST00000389680.2 linkn.-32T>C upstream_gene_variant 6

Frequencies

Mitomap GenBank
The variant is not present, suggesting it is rare.

Mitomap

Disease(s): Maternally-inherited-epilepsy-/-mito-tubulointerstitial-kidney-disease-(MITKD)-/-Gitelman-like-syndrome,Maternally-inherited-epilepsy
Status: Cfrm-[LP],Reported
Publication(s): 31965079, 20142618

ClinVar

Significance: Likely pathogenic
Submissions summary: Pathogenic:5
Revision: reviewed by expert panel
LINK: link

Submissions by phenotype

Mitochondrial disease Pathogenic:2
May 04, 2022
Mendelics
Significance:Pathogenic
Review Status:criteria provided, single submitter
Collection Method:clinical testing

- -

Jun 30, 2022
ClinGen Mitochondrial Disease Nuclear and Mitochondrial Variant Curation Expert Panel, ClinGen
Significance:Likely pathogenic
Review Status:reviewed by expert panel
Collection Method:curation

The m.616T>C variant in MT-TF has been reported in at least 12 individuals from six families with features of a primary mitochondrial disease. Affected individuals had variable ages of onset (first few months of life with delays or seizures at 10 months old to late teenage years with renal disease or epilepsy). Several individuals had chronic kidney disease or renal failure; some even had transplants with non-recurrence of disease post-transplant. Other symptoms reported include developmental delay, epilepsy, status epilepticus (EPC), and myoclonus. Muscle biopsy revealed COX negative fibers. Heteroplasmy levels were the same in all affected probands as the variant was present at homoplasmy or > 97% in all tissues. Of note, some healthy family members had the variant at lower heteroplasmy levels but in at least one healthy family member, the variant was present at a heteroplasmy level as high as 92% (PS4_moderate; PMIDs: 31722346, 28267784, 20142618). There are no reports of de novo occurrence of this variant. This variant segregated with disease in multiple affected members in multiple families and several healthy family members had lower or undetectable levels of the variant (PP1_moderate; PMIDs: 31722346, 28267784, 20142618). This variant is absent in the GenBank dataset, Helix dataset, and gnomAD v3.1.2 (PM2_supporting). There is one cybrid study for this variant however the cybrid also had another mtDNA variant precluding scoring for PS3. There are no single fiber studies or other functional assays reported for this variant. The computational predictor MitoTIP suggests this variant is pathogenic (83.3 percentile) and HmtVAR predicts it to be pathogenic score of 0.5 (PP3). In summary, this variant meets criteria to be classified as likely pathogenic for primary mitochondrial disease inherited in a mitochondrial manner. This classification was approved by the NICHD/NINDS U24 Mitochondrial Disease Variant Curation Expert Panel on June 13, 2022. Mitochondrial DNA-specific ACMG/AMP criteria applied (PMID: 32906214): PS4_moderate, PP1_moderate, PP3, PM2_supporting. -

Interstitial nephritis Pathogenic:1
Jul 07, 2021
Joint Genome Diagnostic Labs from Nijmegen and Maastricht, Radboudumc and MUMC+
Significance:Pathogenic
Review Status:criteria provided, single submitter
Collection Method:clinical testing

The m.616T>C variant was observed in 1 family affected by tubulo-interstitial kidney disease (Connor et al. 2017). At least two members of this family were later found to additionally suffer from hypomagnesemia and hypokalemia.(Viering et al. 2021) The homoplasmic variant cosegregated with disease. The variant was scored as pathogenic based on the system published by Wong et al. (2020): PS5, PM7, PM9, PM10. -

Epilepsy, mitochondrial Pathogenic:1
Feb 09, 2010
OMIM
Significance:Pathogenic
Review Status:no assertion criteria provided
Collection Method:literature only

- -

MELAS syndrome Pathogenic:1
Jul 12, 2019
Wong Mito Lab, Molecular and Human Genetics, Baylor College of Medicine
Significance:Pathogenic
Review Status:criteria provided, single submitter
Collection Method:clinical testing

The NC_012920.1:m.616T>C variant in MT-TF gene is interpreted to be a Pathogenic variant based on the modified ACMG guidelines (unpublished). This variant meets the following evidence codes reported in the guidelines: PS5, PM7, PM9, PM10 -

Computational scores

Source: dbNSFP v4.3

Name
Calibrated prediction
Score
Prediction
Mitotip
Pathogenic
17
Hmtvar
Pathogenic
0.50
PhyloP100
3.7

Publications

Other links and lift over

dbSNP: rs387906420; hg19: chrM-618; API