KNL1

Chr 15AR

kinetochore scaffold 1

Also known as: AF15Q14, CASC5, CT29, D40, MCPH4, PPP1R55, Spc7, hKNL-1

The protein functions as a scaffold component of the outer kinetochore complex that mediates chromosome-microtubule attachments during cell division and recruits spindle assembly checkpoint proteins to ensure proper chromosome segregation. Mutations cause autosomal recessive primary microcephaly-4, a disorder characterized by severely reduced brain size present from birth. The gene shows high constraint against loss-of-function variants (LOEUF 0.314), indicating that complete loss of protein function is poorly tolerated.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 0.311 OMIM phenotype
Clinical SummaryKNL1
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.78) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
11 unique Pathogenic / Likely Pathogenic· 81 VUS of 200 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.31LOEUF
pLI 0.783
Z-score 6.86
OE 0.21 (0.150.31)
Highly constrained

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

Missense Constraint
-0.01Z-score
OE missense 1.00 (0.951.05)
1166 obs / 1165.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.21 (0.150.31)
00.351.4
Missense OE1.00 (0.951.05)
00.61.4
Synonymous OE0.97
01.21.6
LoF obs/exp: 19 / 88.8Missense obs/exp: 1166 / 1165.2Syn Z: 0.44
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongKNL1-related primary microcephalyLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.4090th %ile
GOF
0.15100th %ile
LOF
0.65top 25%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

200 submitted variants in ClinVar

Classification Summary

Pathogenic4
Likely Pathogenic7
VUS81
Likely Benign50
Benign29
4
Pathogenic
7
Likely Pathogenic
81
VUS
50
Likely Benign
29
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
3
0
1
0
4
Likely Pathogenic
6
1
0
0
7
VUS
1
75
5
0
81
Likely Benign
0
2
24
24
50
Benign
0
0
29
0
29
Total10785924171

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

KNL1 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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