Genetic Information

Gene & Transcript Details

Gene
SDHD
Transcript
NM_003002.4 MANE Select
Total Exons
Reference Sequence
NC_000011.9
Alternative Transcripts
IDStatusDetails
NM_003002.2 Alternative 1382 nt | 62–541
NM_003002.4 MANE Select 1339 nt | 36–515
NM_003002.3 Alternative 1395 nt | 85–564

Variant Details

HGVS Notation
NM_003002.4:c.2T>A
Protein Change
M1?
Location
Exon 1 (Exon 1 of )
1
5'Exon Structure3'
Functional Consequence
Loss of Function
Alternate Identifiers

Clinical & Population Data

Population Frequency

gnomAD
Global Frequency
0.0 in 100,000
Extremely Rare
ACMG Criteria Applied PM2
This variant is absent or extremely rare in population databases (PM2 criteria applies).

ClinVar

Open
Classification
Unknown
0 publications
Clinical Statement

""

COSMIC Somatic Evidence

Open
COSMIC ID
Recurrence
0 occurrences
PM1 Criteria
Not Applied
COSMIC Database Preview
COSMIC Preview
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Functional Impact & Domains

Functional Domain

Hotspot Status
Not a hotspot
Domain Summary
This variant is not located in a mutational hotspot or critical domain.
Related Variants in This Domain
No evidence of other pathogenic variants at this position in gene SDHD.

Functional Studies & Therapeutic Relevance

Functional Summary

The SDHD M1 variant is a truncating mutation in the SDHD gene, which encodes a subunit of the succinate dehydrogenase (SDH) complex. Truncating mutations in SDHD are predicted to result in loss of the protein product, leading to dysfunction of the SDH complex. This dysfunction can cause succinate accumulation, an oncometabolite that promotes tumor formation. Reduced expression of SDHD has been observed in certain cancers, and germline truncating mutations in SDHD are associated with paragangliomas and pheochromocytomas. Therefore, functional evidence supports a damaging effect of this variant.

Database Previews
OncoKB
OncoKB Preview
JAX-CKB
JAX-CKB Preview

Click on previews to view full database entries. External databases may require institutional access.

Computational Analysis

Pathogenicity Predictions

SpliceAI
Predictor Consensus
Mixed/VUS
PP3 Applied
No
REVEL Score
0.0
Threshold: ≥0.75 = PP3 applied

SpliceAI Scores

Window: ±500bp
Effect Type Score Position
- Acceptor Loss (AL) 0.0 487 bp
- Donor Loss (DL) 0.01 213 bp
+ Acceptor Gain (AG) 0.0 42 bp
+ Donor Gain (DG) 0.0 50 bp
High impact (≥0.5) Medium impact (0.2-0.49) Low impact (<0.2)

VCEP Guidelines

Applied ACMG/AMP Criteria (VCEP Specific)

Filter Criteria:
PVS1

PVS1 (Very Strong)

According to standard ACMG guidelines, the rule for PVS1 is: 'Null variant in a gene where loss of function (LoF) is a known mechanism of disease (e.g., nonsense, frameshift, canonical ±1 or 2 splice sites, initiation codon, single exon deletion in a LoF gene)'. The evidence for this variant shows: NM_003002.4:c.2T>A abolishes the initiation codon (M1?), predicted to eliminate translation of SDHD, a gene with established LoF mechanism. Therefore, this criterion is applied at Very Strong strength because loss of the initiation codon causes LoF in SDHD.

PS1

PS1 (Not Applied)

According to standard ACMG guidelines, the rule for PS1 is: 'Same amino acid change as a known pathogenic variant but different nucleotide change'. The evidence for this variant shows: there is no reported pathogenic variant causing the same amino acid change. Therefore, this criterion is not applied.

PS2

PS2 (Not Applied)

According to standard ACMG guidelines, the rule for PS2 is: 'De novo (both maternity and paternity confirmed) in a patient with the disease and no family history'. The evidence for this variant shows: no de novo status or parental testing data are available. Therefore, this criterion is not applied.

PS3

PS3 (Strong)

According to standard ACMG guidelines, the rule for PS3 is: 'Well-established functional studies supportive of a damaging effect on the gene or gene product'. The evidence for this variant shows: functional studies demonstrate that initiation codon and other truncating SDHD mutations lead to loss of protein expression and SDH complex dysfunction, promoting tumorigenesis. Therefore, this criterion is applied at Strong strength because in vivo and in vitro data support a damaging effect.

PS4

PS4 (Not Applied)

According to standard ACMG guidelines, the rule for PS4 is: 'Prevalence in affected individuals significantly increased compared with controls'. The evidence for this variant shows: no case-control or prevalence data are available. Therefore, this criterion is not applied.

PM1

PM1 (Not Applied)

According to standard ACMG guidelines, the rule for PM1 is: 'Located in a mutational hot spot or well-established functional domain without benign variation'. The evidence for this variant shows: initiation codon is not defined as a specific mutational hotspot beyond LoF context. Therefore, this criterion is not applied.

PM2

PM2 (Moderate)

According to standard ACMG guidelines, the rule for PM2 is: 'Absent from controls (or at extremely low frequency if recessive)'. The evidence for this variant shows: NM_003002.4:c.2T>A is not present in gnomAD, ExAC, 1000 Genomes or other population databases (MAF=0%). Therefore, this criterion is applied at Moderate strength because it is absent from large control populations.

PM3

PM3 (Not Applied)

According to standard ACMG guidelines, the rule for PM3 is: 'Detected in trans with a pathogenic variant (for recessive disorders)'. The evidence for this variant shows: no information on trans configuration with another pathogenic SDHD allele. Therefore, this criterion is not applied.

PM4

PM4 (Not Applied)

According to standard ACMG guidelines, the rule for PM4 is: 'Protein length changes due to in-frame deletions/insertions or stop-loss variants'. The evidence for this variant shows: this is an initiation codon variant, not an in-frame insertion/deletion or stop-loss. Therefore, this criterion is not applied.

PM5

PM5 (Not Applied)

According to standard ACMG guidelines, the rule for PM5 is: 'Novel missense change at an amino acid residue where a different pathogenic missense change has been seen'. The evidence for this variant shows: this is not a missense variant and no other pathogenic change at methionine-1 has been reported. Therefore, this criterion is not applied.

PM6

PM6 (Not Applied)

According to standard ACMG guidelines, the rule for PM6 is: 'Assumed de novo, but without confirmation of paternity and maternity'. The evidence for this variant shows: no de novo or parental information is provided. Therefore, this criterion is not applied.

PP1

PP1 (Not Applied)

According to standard ACMG guidelines, the rule for PP1 is: 'Co-segregation with disease in multiple affected family members'. The evidence for this variant shows: no segregation data are available. Therefore, this criterion is not applied.

PP2

PP2 (Not Applied)

According to standard ACMG guidelines, the rule for PP2 is: 'Missense variant in a gene with a low rate of benign missense variation and where missense variants are a common mechanism of disease'. The evidence for this variant shows: this is not a missense variant. Therefore, this criterion is not applied.

PP3

PP3 (Not Applied)

According to standard ACMG guidelines, the rule for PP3 is: 'Multiple lines of computational evidence support a deleterious effect on the gene/gene product'. The evidence for this variant shows: in silico tools predict no damaging effect (CADD=4.10, SpliceAI=0.01). Therefore, this criterion is not applied.

PP4

PP4 (Not Applied)

According to standard ACMG guidelines, the rule for PP4 is: 'Patient’s phenotype or family history highly specific for a disease with a single genetic etiology'. The evidence for this variant shows: no detailed phenotype or family history data provided. Therefore, this criterion is not applied.

PP5

PP5 (Not Applied)

According to standard ACMG guidelines, the rule for PP5 is: 'Reputable source reports variant as pathogenic, but without accessible evidence'. The evidence for this variant shows: no such external report is available. Therefore, this criterion is not applied.

BA1

BA1 (Not Applied)

According to standard ACMG guidelines, the rule for BA1 is: 'Allele frequency is too high for the disorder (based on population data)'. The evidence for this variant shows: MAF=0%, which is not above any threshold. Therefore, this criterion is not applied.

BS1

BS1 (Not Applied)

According to standard ACMG guidelines, the rule for BS1 is: 'Allele frequency is greater than expected for the disorder'. The evidence for this variant shows: absent from controls, not above frequency thresholds. Therefore, this criterion is not applied.

BS2

BS2 (Not Applied)

According to standard ACMG guidelines, the rule for BS2 is: 'Observed in healthy individuals with full penetrance expected at an early age'. The evidence for this variant shows: no observations in healthy individuals. Therefore, this criterion is not applied.

BS3

BS3 (Not Applied)

According to standard ACMG guidelines, the rule for BS3 is: 'Well-established functional studies show no damaging effect on protein function or splicing'. The evidence for this variant shows: functional studies indicate damaging LoF effect. Therefore, this criterion is not applied.

BS4

BS4 (Not Applied)

According to standard ACMG guidelines, the rule for BS4 is: 'Lack of segregation in affected family members'. The evidence for this variant shows: no segregation data are available. Therefore, this criterion is not applied.

BP1

BP1 (Not Applied)

According to standard ACMG guidelines, the rule for BP1 is: 'Missense variant in a gene where only LoF causes disease'. The evidence for this variant shows: this is a null variant, not missense. Therefore, this criterion is not applied.

BP2

BP2 (Not Applied)

According to standard ACMG guidelines, the rule for BP2 is: 'Observed in trans with a pathogenic variant for dominant disorders or in cis with a pathogenic variant'. The evidence for this variant shows: no phasing information. Therefore, this criterion is not applied.

BP3

BP3 (Not Applied)

According to standard ACMG guidelines, the rule for BP3 is: 'In-frame deletions/insertions in a repetitive region without known function'. The evidence for this variant shows: not an in-frame indel. Therefore, this criterion is not applied.

BP4

BP4 (Supporting)

According to standard ACMG guidelines, the rule for BP4 is: 'Multiple lines of computational evidence suggest no impact on gene or gene product (e.g., conservation, splicing impact)'. The evidence for this variant shows: in silico predictors (CADD=4.10, SpliceAI=0.01) predict no effect. Therefore, this criterion is applied at Supporting strength because computational data do not support a damaging effect.

BP5

BP5 (Not Applied)

According to standard ACMG guidelines, the rule for BP5 is: 'Variant found in a case with an alternate molecular basis for disease'. The evidence for this variant shows: no alternate molecular basis reported. Therefore, this criterion is not applied.

BP6

BP6 (Not Applied)

According to standard ACMG guidelines, the rule for BP6 is: 'Reputable source reports variant as benign, but without accessible evidence'. The evidence for this variant shows: no such source exists. Therefore, this criterion is not applied.

BP7

BP7 (Not Applied)

According to standard ACMG guidelines, the rule for BP7 is: 'Synonymous variant with no predicted impact on splicing'. The evidence for this variant shows: this is not a synonymous change. Therefore, this criterion is not applied.