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. Author manuscript; available in PMC: 2026 Mar 3.
Published in final edited form as: Mol Cell. 2025 Dec 30;86(1):41–59.e15. doi: 10.1016/j.molcel.2025.12.003

Figure 3. CRASP-seq identifies ZNF207 as a regulator of progerin aberrant splicing.

Figure 3.

(A) Heatmap of ΔPSI for mutant LMNA CRASP-seq screen hits in HAP1, RPE1, and HepG2 cells.

(B) Schematic of ZNF207 protein structure, highlighting the C2H2 zinc-finger (ZnF) domains, the charged helical region, low-complexity regions, and the Gle2-binding-sequence (GLEBS) motif.

(C) RT-PCR of LMNA splicing in RNA from HGPS patient-derived fibroblasts treated with three independent siRNAs. Quantifications of PSI values from three independent experiments are presented as mean ± standard deviation (SD). ****p value < 0.0001; Dunnett’s multiple comparisons test.

(D) RT-PCR of LMNA splicing in RNA from HGPS patient-derived fibroblasts after ZNF207 knockdown and rescue with siRNA-resistant ZNF207 ORF. Quantification of PSI values from three independent experiments is presented as mean ± SD. ****p value < 0.0001; Dunnett’s multiple comparisons test.

(E) Western blot of lamins in HGPS fibroblasts with siRNA-resistant 3×FLAG-ZNF207 or empty vector, with/without siZNF207. Quantification normalized to β-actin and siControl from three independent experiments is presented as mean ± SD. *p value < 0.05, ****p value < 0.0001; Uncorrected Fisher’s least significant difference (LSD) following one-way ANOVA.