Supplementary Fig. 11: Characterization of Adamts19 mouse alleles based on scRNA-seq data.
From: Loss of ADAMTS19 causes progressive non-syndromic heart valve disease

A) Spliced reads spanning the exon-intron junction between endogenous exon 2 and 3 of wild-type Adamts19 are readily detected in homozygous wild-type mice but absent in tm4a and tm4b alleles. B) Unspliced reads, mapping to endogenous exon 3 of Adamts19 are quantified. Homozygous wild-type and homozygous tm4a mice have unspliced reads on exon 3, while this exon is deleted in homozygous tm4b mice and thus has no reads in this genotype. C) Spliced reads between the endogenous exon 2 of Adamts19 and the inserted lacZ cassette (En2 exon, IRES, lacZ) with a strong splice acceptor of the En2 gene at the 5’ end of the cassette is shown. Boxplots show the interquartile range (IQR, 25th to 75th percentile) with 50th percentile as solid line. Whiskers represent 1.5 * IQR. D) Expression of Adamts19 and LacZ over all cell types for Adamts19+/+ (WT), tm4a and tm4b (Adamts19KO/KO) single-cell transcriptomes. N = 7 for Adamts19+/+ and n = 8 for Adamts19KO/KO.