Abstract
MERTK mutations are associate with rod-cone dystrophies. To enable investigations into the mechanism of this disease, we generated a cell line resource of H9 human embryonic stem cells harboring large fragment deletion mutation in a homozygous state in exon 19 of the MERTK gene. This subline expressed pluripotent stem cell markers, presented a normal karyotype, and preserved the ability to differentiate into endodermal, mesodermal, and ectodermal lineages.