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. Author manuscript; available in PMC: 2021 Dec 28.
Published in final edited form as: Cancer Cell. 2015 Apr 23;27(5):658–670. doi: 10.1016/j.ccell.2015.03.017

Figure 6: Deep whole RNA sequencing showed splicing defects in DDX41 deficient cells.

Figure 6:

(A) Increased exon skipping (top) and retention (bottom) in patients with DDX41 defects are indicated by an excess of green reads and red reads, respectively. The center panel shows a scatter plot of exon skipping in RNA isolated from control cells versus RNA from DDX41 defective mutant cells. Lines show the 10% difference cutoff limit used to select the most frequently affected exons.

(B) Deep RNA sequencing was performed for blasts from patients with DDX41 mutations, deletions and wild-type to analyze altered splicing. The bar diagrams indicate the top 10 genes significantly more skipped in DDX41 defects (top) and in DDX41 wild-type (bottom). The arrow indicates the 13% difference of exon skipping in the ZMYM2 gene when comparing DDX41 defect and wild-type samples.

(C) Exon 3 of ZMYM2 was skipped in DDX41 deficient cells as demonstrated by the read counts from deep sequencing.

(D) RT-PCR was performed in K562 cells, CD34+ progenitors and U937 cells to evaluate ZMYM2 exon 3 skipping compared with controls. Depicted is the skip:retain intensity ratio for wild-type and DDX41 knockdown/overexpressing samples. Each bar represents the mean±SEM of 3 independent experiments.

See also Figure S7/Table S6