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Repair of the TGFBI gene in human corneal keratocytes derived from a granular corneal dystrophy patient via CRISPR/Cas9-induced homology-directed repair.
- Source :
-
Scientific reports [Sci Rep] 2017 Dec 01; Vol. 7 (1), pp. 16713. Date of Electronic Publication: 2017 Dec 01. - Publication Year :
- 2017
-
Abstract
- Granular corneal dystrophy (GCD) is an autosomal dominant hereditary disease in which multiple discrete and irregularly shaped granular opacities are deposited in the corneal stroma. GCD is caused by a point mutation in the transforming growth factor-β-induced (TGFBI) gene, located on chromosome 5q31. Here, we report the first successful application of CRISPR-Cas9-mediated genome editing for the correction of a TGFBI mutation in GCD patient-derived primary corneal keratocytes via homology-directed repair (HDR). To correct genetic defects in GCD patient cells, we designed a disease-specific guide RNA (gRNA) targeting the R124H mutation of TGFBI, which causes GCD type 2 (GCD2). An R124H mutation in primary human corneal keratocytes derived from a GCD2 patient was corrected by delivering a CRISPR plasmid expressing Cas9/gRNA and a single-stranded oligodeoxynucleotide HDR donor template in vitro. The gene correction efficiency was 20.6% in heterozygous cells and 41.3% in homozygous cells. No off-target effects were detected. These results reveal a new therapeutic strategy for GCD2; this method may also be applicable to other heredity corneal diseases.
- Subjects :
- Base Sequence
Cells, Cultured
Corneal Dystrophies, Hereditary metabolism
Corneal Dystrophies, Hereditary pathology
Corneal Keratocytes cytology
Corneal Keratocytes metabolism
Gene Editing
Heterozygote
Homozygote
Humans
Mutagenesis, Site-Directed
Sequence Analysis, DNA
CRISPR-Cas Systems genetics
Transforming Growth Factor beta genetics
Subjects
Details
- Language :
- English
- ISSN :
- 2045-2322
- Volume :
- 7
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Scientific reports
- Publication Type :
- Academic Journal
- Accession number :
- 29196743
- Full Text :
- https://doi.org/10.1038/s41598-017-16308-2