When the genome bluffs: a tandem duplication event during generation of a novel Agmo knockout mouse model fools routine genotyping.

Alkylglycerol monooxygenase Ether lipid metabolism Genomic structural variation Homologous recombination Mouse models

Journal

Cell & bioscience
ISSN: 2045-3701
Titre abrégé: Cell Biosci
Pays: England
ID NLM: 101561195

Informations de publication

Date de publication:
16 Mar 2021
Historique:
received: 01 12 2020
accepted: 25 02 2021
entrez: 17 3 2021
pubmed: 18 3 2021
medline: 18 3 2021
Statut: epublish

Résumé

Genome editing in mice using either classical approaches like homologous recombination or CRISPR/Cas9 has been reported to harbor off target effects (insertion/deletion, frame shifts or gene segment duplications) that lead to mutations not only in close proximity to the target site but also outside. Only the genomes of few engineered mouse strains have been sequenced. Since the role of the ether-lipid cleaving enzyme alkylglycerol monooxygenase (AGMO) in physiology and pathophysiology remains enigmatic, we created a knockout mouse model for AGMO using EUCOMM stem cells but unforeseen genotyping issues that did not agree with Mendelian distribution and enzyme activity data prompted an in-depth genomic validation of the mouse model. We report a gene segment tandem duplication event that occurred during the generation of an Agmo knockout-first allele by homologous recombination. Only low homology was seen between the breakpoints. While a single copy of the recombinant 18 kb cassette was integrated correctly around exon 2 of the Agmo gene, whole genome nanopore sequencing revealed a 94 kb duplication in the Agmo locus that contains Agmo wild-type exons 1-3. The duplication fooled genotyping by routine PCR, but could be resolved using qPCR-based genotyping, targeted locus amplification sequencing and nanopore sequencing. Despite this event, this Agmo knockout mouse model lacks AGMO enzyme activity and can therefore be used to study its physiological role. A duplication event occurred at the exact locus of the homologous recombination and was not detected by conventional quality control filters such as FISH or long-range PCR over the recombination sites. Nanopore sequencing provides a cost convenient method to detect such underrated off-target effects, suggesting its use for additional quality assessment of gene editing in mice and also other model organisms.

Sections du résumé

BACKGROUND BACKGROUND
Genome editing in mice using either classical approaches like homologous recombination or CRISPR/Cas9 has been reported to harbor off target effects (insertion/deletion, frame shifts or gene segment duplications) that lead to mutations not only in close proximity to the target site but also outside. Only the genomes of few engineered mouse strains have been sequenced. Since the role of the ether-lipid cleaving enzyme alkylglycerol monooxygenase (AGMO) in physiology and pathophysiology remains enigmatic, we created a knockout mouse model for AGMO using EUCOMM stem cells but unforeseen genotyping issues that did not agree with Mendelian distribution and enzyme activity data prompted an in-depth genomic validation of the mouse model.
RESULTS RESULTS
We report a gene segment tandem duplication event that occurred during the generation of an Agmo knockout-first allele by homologous recombination. Only low homology was seen between the breakpoints. While a single copy of the recombinant 18 kb cassette was integrated correctly around exon 2 of the Agmo gene, whole genome nanopore sequencing revealed a 94 kb duplication in the Agmo locus that contains Agmo wild-type exons 1-3. The duplication fooled genotyping by routine PCR, but could be resolved using qPCR-based genotyping, targeted locus amplification sequencing and nanopore sequencing. Despite this event, this Agmo knockout mouse model lacks AGMO enzyme activity and can therefore be used to study its physiological role.
CONCLUSIONS CONCLUSIONS
A duplication event occurred at the exact locus of the homologous recombination and was not detected by conventional quality control filters such as FISH or long-range PCR over the recombination sites. Nanopore sequencing provides a cost convenient method to detect such underrated off-target effects, suggesting its use for additional quality assessment of gene editing in mice and also other model organisms.

Identifiants

pubmed: 33726865
doi: 10.1186/s13578-021-00566-9
pii: 10.1186/s13578-021-00566-9
pmc: PMC7962373
doi:

Types de publication

Journal Article

Langues

eng

Pagination

54

Subventions

Organisme : Austrian Science Fund
ID : P30800
Organisme : Austrian Science Fund
ID : P33333
Organisme : Austrian Science Fund FWF
ID : P 30800
Pays : Austria
Organisme : Austrian Science Fund FWF
ID : P 28769
Pays : Austria
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1039 A03
Organisme : British Heart Foundation
ID : RG/12/5/29576
Pays : United Kingdom
Organisme : Austrian Science Fund
ID : P28769
Organisme : British Heart Foundation
ID : CH/16/1/32013
Pays : United Kingdom

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Auteurs

Sabrina Sailer (S)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Stefan Coassin (S)

Institute of Genetic Epidemiology, Department of Genetics and Pharmacology, Medical University of Innsbruck, Innsbruck, Austria.

Katharina Lackner (K)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Caroline Fischer (C)

Institute of Clinical Pharmacology of the Medical Faculty, Goethe-University, Frankfurt (Main), Germany.

Eileen McNeill (E)

Wellcome Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Division of Cardiovascular Medicine, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.

Gertraud Streiter (G)

Institute of Genetic Epidemiology, Department of Genetics and Pharmacology, Medical University of Innsbruck, Innsbruck, Austria.

Christian Kremser (C)

Department of Radiology, Medical University of Innsbruck, Innsbruck, Austria.

Manuel Maglione (M)

Department of Visceral, Transplant and Thoracic Surgery, Medical University of Innsbruck, Innsbruck, Austria.

Catherine M Green (CM)

Wellcome Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.

Daniela Moralli (D)

Wellcome Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.

Alexander R Moschen (AR)

Department of Internal Medicine I, Gastroenterology, Endocrinology and Metabolism, Medical University of Innsbruck, Innsbruck, Austria.

Markus A Keller (MA)

Institute of Human Genetics, Medical University of Innsbruck, Innsbruck, Austria.

Georg Golderer (G)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Gabriele Werner-Felmayer (G)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Irmgard Tegeder (I)

Institute of Clinical Pharmacology of the Medical Faculty, Goethe-University, Frankfurt (Main), Germany.

Keith M Channon (KM)

Wellcome Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Division of Cardiovascular Medicine, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.

Benjamin Davies (B)

Wellcome Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.

Ernst R Werner (ER)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

Katrin Watschinger (K)

Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria. katrin.watschinger@i-med.ac.at.
Institute of Biological Chemistry, Biocenter, Medical University of Innsbruck, Innrain 80, 6020, Innsbruck, Austria. katrin.watschinger@i-med.ac.at.

Classifications MeSH