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Published Erratum
. 2025 Mar 6;148(3):e16-e20.
doi: 10.1093/brain/awae353.

Correction to: Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

No authors listed
Published Erratum

Correction to: Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

No authors listed. Brain. .
No abstract available

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Figures

Figure 1
Figure 1
Proliferation of schwannoma cells in the DRG and VG is dependent upon both YAP and TAZ proteins. (A–H) Images of DRG (A–D) and VG (E–H) from 5-month-old mice stained for EdU and neurofilament (NF); sections were counterstained with Hoechst to reveal nuclei (Ho). Arrows indicate EdU-positive nuclei in the areas of the ganglia in close proximity to the neuronal cell bodies; note fewer proliferating cells in NF2/YAP (C and G) and NF2/TAZ (D and H) than in NF2 single null (B and F) ganglia. (I and J) Quantification of EdU-positive cells per area of ganglion tissue of DRG (I) and VG (J). Note significant decreases in proliferation in both NF2/YAP and NF2/TAZ ganglia. (K–R) Staining of DRG sections from 9-month-old control (NF2fl/flCRE-; K and O), NF2 single null (NF2fl/flCRE+; L and P), NF2/YAP double null (NF2fl/fl/YAPfl/flCRE+; M and Q) and NF2/TAZ double null (NF2fl/fl/TAZfl/flCRE+; N and R) animals. Panels K–N show staining with YAP antibody; panels O–R with TAZ antibody. Note raised nuclear expression of YAP in NF2 single (L; arrows) and NF2/TAZ double (N; arrows) null tissue, which is lost in NF2/YAP double null tissue (M; arrows). For TAZ staining, note raised nuclear TAZ expression in NF2 single (P; arrows) and NF2/YAP double (Q; arrows) null tissue, which is not present in NF2/TAZ double null DRG tissue (R; arrows). A–D and I, n = 4; E–H and J, n = 3; K–R, n = 3 for each genotype examined. Data presented in graphs are means±SEM using one-way ANOVA with Bonferroni's multiple comparison tests. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant. Scale bars = A–H 75 µm, K–R 50 µm.
Figure 2
Figure 2
Treatment of mice with VT1 or VT2 TEAD auto-palmitoylation inhibitors significantly inhibits proliferation of vestibular schwannoma tumours in vivo. Data from 3-month-old NF2fl/fl-CRE- (CRE-) and NF2fl/fl-CRE+ (CRE+) animals treated with vehicle (Veh), 10 mg/kg/day VT1 or 30 mg/kg/day VT2 by oral gavage for 21 consecutive days. (A–H) Both VT1 and VT2 significantly block tumour cell growth as measured by EdU incorporation in vestibular ganglion tissue. (A–F) Representative images of vestibular ganglion from CRE- and CRE+ 3-month-old animals treated with either vehicle (A, B, D and E), VT1 (C) or VT2 (F). Note no EdU-positive cells are seen in CRE- animals with vehicle and that for CRE+ animals, numbers of EdU-positive cells (indicated by arrows) are reduced upon treatment with either VT1 (C) or VT2 (F). (G and H) Quantification of numbers of EdU-positive cells per area of ganglion tissue from animals treated with vehicle (Veh) or VT1 (Drug, G) or VT2 (Drug, H) compounds. Note significant decreases in proliferation in CRE+ animals treated with either VT1 or VT2. (I–N) Representative western blots and quantification to show target engagement of VT1 and VT2 in regulating connective tissue growth factor (CTGF) and TEAD protein expression in sciatic nerve tissue of CRE- and CRE+ mice. I. Western blot of sciatic nerve of 3-month-old mice treated for 21 days with either Vehicle (Veh), VT1 (Drug, I) or Vehicle or VT2 (Drug, L). (J and K) Quantification of western blot in I. (M and N) Quantification of western blot in L. Note significant decrease in TEAD target CTGF by both VT1 and VT2 in sciatic nerve tissue in vivo (J and M) and reduction in TEAD protein expression by VT2 (N) but not by VT1 (K). For data in A–H, n = 4 mice for each genotype and drug treatment. For data in J, K, M and N, n = 3 mice for each genotype and drug treatment. Data presented in graphs are means±SEM using one-way ANOVA with Bonferroni's multiple comparison tests. *P < 0.05; **P < 0.01; ***P < 0.001. Scale bar = 50 µm in A–F.
Figure 3
Figure 3
Treatment of mice with VT auto-palmitoylation inhibitors significantly increases apoptosis and reduces tumour volumes in VG and DRG in 9-month-old NF2fl/fl-CRE+ (NF2fl/fl-CRE+) mice. NF2fl/fl-CRE- (NF2fl/fl-CRE-) and NF2fl/fl-CRE+ animals were treated with vehicle (Veh), 10 mg/kg/day VT1 or 30 mg/kg/day VT2 by oral gavage for 10 or 21 consecutive days. (A–D) Representative brightfield micrographs of three different unilateral VG from: NF2fl/fl-CRE- Veh-treated mice (A), NF2fl/fl-CRE+ Veh-treated mice (B), NF2fl/fl-CRE+ VT1-treated mice (C) and NF2fl/fl-CRE+ VT2-treated mice (D), all mice were treated for 21 consecutive days. Scale bar = 20 µm. (E) Quantification of average bilateral VG volume in A–D, for NF2fl/fl-CRE- Veh-treated mice (n = 6 ganglia, n = 3 mice), NF2fl/fl-CRE+ Veh-treated mice (n = 4 ganglia, n = 3 mice), NF2fl/fl-CRE+ VT1-treated mice (n = 3 ganglia, n = 3 mice) and NF2fl/fl-CRE+ VT2-treated mice (n = 3 ganglia, n = 3 mice). (F) Quantification of average bilateral lumbar 4 DRG volume, for NF2fl/fl-CRE- and NF2fl/fl-CRE+ Veh-treated mice (n = 8 ganglia, n = 3 mice), for NF2fl/fl-CRE+ VT1- and NF2fl/fl-CRE+ VT2-treated mice (n = 3 ganglia, n = 3 mice). (G–R) Representative immunofluorescence of n = 3 different VGs with in situ apoptosis detected by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay, following oral gavage with either vehicle or 30 mg/kg/day VT2 for 10 days. TUNEL+ nuclei (arrows; J, L, P and R) were significantly increased in NF2fl/fl-CRE+ VT2-treated mice compared to NF2fl/fl-CRE+ Veh-treated mice. Neurofilament (NF; H and K) counterstain (merged with Hoechst counterstain (I and L) reveals increased apoptosis in cells surrounding neuronal cell bodies of the VG in NF2fl/fl-CRE+ VT2-treated mice. S100 counterstain (N and Q merged with Hoechst counterstain (O and R) reveals apoptosis is increased in S100+ schwannoma cells of NF2fl/fl-CRE+ VT2-treated mice. Scale bars = 20 µm. (S and T) Quantification of TUNEL+ cells/100 mm2 in VG (S) and DRG (T). In E and F, data presented as mean±SEM using one-way ANOVA with Tukey's multiple comparisons tests. In S and T, data presented as mean±SEM using Brown–Forsythe and Welch ANOVA with Dunnett's T3 multiple comparisons test. **P < 0.01; ***P < 0.001; ns = non-significant.
Supplementary Figure 3
Supplementary Figure 3
Treatment of mice with VT1 or VT2 TEAD auto-palmitoylation inhibitors significantly inhibits growth of dorsal root ganglion (DRG) schwannoma tumours in vivo. Data from 3 month old NF2fl/fl PostnCRE- (CRE-) and NF2fl/fl PostnCRE+ (CRE+) animals treated with vehicle (Veh), 10mg/kg/day VT1 or 30mg/kg/day VT2 by oral gavage for 21 consecutive days. A-H. Both VT1 and VT2 significantly block tumour cell growth as measured by EdU incorporation in DRG tissue. A-F. Images of DRGs from CRE- and CRE+ animals treated with either vehicle (A, B, D and E), VT1 (C) or VT2 (F). Note that for CRE+ animals, numbers of EdU positive cells (indicated by arrows) are reduced upon treatment with either VT1 (C) or VT2 (F). G, H. Quantification of numbers of EdU positive cells per area of ganglion tissue from animals treated with vehicle (Veh.) or VT1 (Drug; G) or VT2 (Drug; H) compounds. Note significant decreases in proliferation in CRE+ animals treated with either VT1 or VT2. For data in A-H, n = 4 mice for each genotype and drug treatment. Data presented in graphs are means ±SEM. Analysis was done using one way ANOVA with Bonferroni's multiple comparison tests. *P < 0.05; **P < 0.01; ***P < 0.001. Scale bar: 200 µm.
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