On this page
⚠ Educational content only Not medical or genetic advice. Speak with a healthcare provider or genetic counsellor before acting on anything here.

COLQ

collagen like tail subunit of asymmetric acetylcholinesterase

The COLQ gene provides instructions for the acetylcholinesterase collagenic tail peptide, a protein crucial for proper function of the neuromuscular junction. COLQ encodes a subunit that anchors acetylcholinesterase, an enzyme involved in neurotransmission, to muscle cells.

Chromosome 3p25.1 Autosomal recessive HGNC:2226 Tier C
COLQ 3p25.1 p arm q arm 3

COLQ is located on the short (p) arm of chromosome 3, at band 3p25.1. Arm ratio per GRCh38 - banding schematic.

Explore chromosome 3 in the library →

Available at Jeen Health

Clinical tests that include this

Overview

The COLQ gene, also known as collagen like tail subunit of asymmetric acetylcholinesterase, provides the genetic blueprint for a protein called the acetylcholinesterase collagenic tail peptide. This protein plays a fundamental role in the neuromuscular junction, which is the specialised connection point between nerve cells and muscle cells where signals are transmitted to initiate muscle movement. Proper function of COLQ is vital for efficient communication between nerves and muscles.

What the gene does

The protein produced from the COLQ gene is essential for regulating nerve-to-muscle signalling by anchoring acetylcholinesterase (AChE) to the muscle cell membrane at the neuromuscular junction. The acetylcholinesterase collagenic tail peptide consists of three identical subunits. Each of these subunits binds to a bundle of four AChE proteins, effectively securing them in place. AChE is responsible for breaking down the neurotransmitter acetylcholine, thereby controlling the duration and strength of muscle contraction signals. By localising AChE, the COLQ protein ensures precise and timely termination of nerve impulses, allowing for coordinated muscle function.

Video: Genetics 101

Chromosome location

The COLQ gene is situated on chromosome 3. Specifically, its chromosomal location is 3p25.1. This region of the chromosome contains the genetic information necessary for the synthesis of the acetylcholinesterase collagenic tail peptide.

Protein structure

The COLQ protein is composed of 455 amino acids. Key regions and domains include a PRAD region spanning amino acids 51-67, and a Disordered region from amino acids 90-282. It also features a Collagen-like 1 domain (amino acids 96-269) and a Collagen-like 2 domain (amino acids 277-291). Additionally, the protein contains two Heparan sulfate proteoglycan binding regions, located at amino acids 130-133 and 235-238, respectively.

Domain map · 455 amino acids
PRAD (51–67)Collagen-like 1 (96–269)Heparan sulfate proteoglycan binding (130–133)Heparan sulfate proteoglycan binding (235–238)Collagen-like 2 (277–291)PRAD51–67Collagen-like 196–269Collagen-like 2277–2911~228455
Region - functional region
Domain - independent functional unit
🧬 Explore 3D structure on AlphaFold
UniProt:Q9Y215Length:455 aaStructure:AlphaFold

Key variants

Variants within the COLQ gene can impact the production or function of the acetylcholinesterase collagenic tail peptide. These genetic changes can lead to an impaired ability of the protein to anchor acetylcholinesterase, subsequently affecting neuromuscular transmission. Understanding these variants is crucial for diagnosing associated conditions.

The table below shows the top 10 pathogenic or likely-pathogenic variants currently classified in ClinVar for COLQ.
View all on ClinVar →

Sample of pathogenic variants

10 pathogenic / likely-pathogenic variants from ClinVar, ranked by review status (expert-panel-reviewed first). This is a sample; recurrent founder variants in a specific population may not appear here - see the full ClinVar listing via the link above.

Variant (HGVS) Protein change Classification Evidence Associated condition
c.1026C>G
single nucleotide variant
p.Asp342Glu Pathogenic/Likely pathogenic ★★☆☆ Synaptic congenital myasthenic syndromes
c.175C>T
single nucleotide variant
p.Pro59Ser Pathogenic/Likely pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.241_242dup
Duplication
p.Asn81fs Pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.631C>T
single nucleotide variant
p.Gln211Ter Pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.700G>T
single nucleotide variant
p.Gly234Ter Pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.827_843del
Deletion
p.Met276fs Pathogenic/Likely pathogenic ★★☆☆ Synaptic congenital myasthenic syndromes
c.893del
Deletion
p.Asn298fs Pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.955-2A>C
single nucleotide variant
- Pathogenic/Likely pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.955-2A>T
single nucleotide variant
- Pathogenic/Likely pathogenic ★★☆☆ Congenital myasthenic syndrome 5
c.992_998del
Deletion
p.Leu331fs Pathogenic/Likely pathogenic ★★☆☆ Congenital myasthenic syndrome

Evidence stars indicate ClinVar review status. Individual variant interpretation should always be performed by a qualified clinical laboratory - many variants remain classified as Variants of Uncertain Significance (VUS) pending more research.

Associated conditions

Pathogenic variants in the COLQ gene are linked to congenital myasthenic syndromes, specifically Congenital myasthenic syndrome (COLQ). These are a group of inherited disorders characterised by muscle weakness and easy fatigability (myasthenia), typically presenting either shortly after birth or during early childhood. The autosomal recessive inheritance pattern means that an individual must inherit two copies of a pathogenic variant, one from each parent, to develop the condition.

Inheritance pattern

Conditions caused by pathogenic COLQ variants typically follow autosomal recessive inheritance.

♀ Carrier parent 1 altered copy ♂ Carrier parent 1 altered copy Affected Carrier Carrier Unaffected Affected Carrier Unaffected Circles = females · Squares = males

When both parents are carriers, each child has a 25% chance of being affected, 50% of being a carrier, and 25% of being unaffected.

Carrier frequency by population How common is heterozygous COLQ carrier status across ancestry groups?

UK clinical status

The COLQ gene is included in several NHS England Genomic Medicine Service national genomic test directories, indicating its clinical relevance within the UK healthcare system. It is listed as 'green' for Arthrogryposis (R83), Congenital myaesthenic syndrome (R80), and Foetal anomalies (R21). A 'green' status signifies that there is sufficient evidence for the gene to be routinely offered on these panels.

Frequently asked questions

What is the primary function of the COLQ gene?

The COLQ gene provides instructions for a protein that anchors acetylcholinesterase (AChE) at the neuromuscular junction. This anchoring is crucial for the efficient breakdown of acetylcholine, which regulates nerve signal transmission to muscles.

Which condition is primarily associated with COLQ gene variants?

Variants in the COLQ gene are primarily associated with congenital myasthenic syndromes, a group of inherited disorders causing muscle weakness and fatigue, often starting in infancy or early childhood.

How is congenital myasthenic syndrome associated with COLQ inherited?

Congenital myasthenic syndrome related to COLQ is inherited in an autosomal recessive pattern. This means an individual must inherit two altered copies of the COLQ gene, one from each parent, to develop the condition.

Educational content. This page is not medical or genetic advice, is not individually reviewed by a clinician for each reader, and should not replace a consultation with a qualified healthcare professional or genetic counsellor. If you are considering genetic testing or acting on a test result, book a consultation.
Data sources Last updated 27 September 2026. Content compiled from HGNC · MedlinePlus Genetics · ClinGen · Genomics England PanelApp · NHS National Genomic Test Directory · ClinVar · UniProt · AlphaFold .