Figure 1: Foxp1 misexpression rescues the Foxp1-mutant phenotype.

Analysis of MN subtypes in the ventral horn of E12.5 Foxp^+/+, Foxp^−/− and Hb9::Foxp1; Foxp1^−/− littermate embryo spinal cords. Scale bar, 50 μm. (a) MN subtypes at cervical levels. Foxp1^−/− embryos had reduced numbers of LMCm (Isl1⁺/Foxp1⁺) and LMCl (Hb9⁺/Lhx1⁺) MNs, while HMC (Hb9⁺/Isl1⁺) and MMC-rhomboideus (Isl1⁺/Lhx3^low) MNs were expanded compared with Foxp1^+/+ embryos¹³. Hb9::Foxp1; Foxp1^−/− embryos had partially restored LMCm and LMCl MNs that resided at the correct lateral positions, and reduced numbers of ectopic HMC and MMC-Rb MNs, compared with Foxp1^−/− embryos. Rb, rhomboideus. (b) MN subtypes at thoracic levels. The loss of PGC (Isl1⁺/nNOS⁺) MNs in Foxp1^−/− embryos was rescued in Hb9::Foxp1; Foxp1^−/− embryos. (c) Quantification of MN percentages at cervical levels (mean±s.e.m.; n=3 sections averaged per embryo, 3 embryos per genotype; two-way analysis of variance (ANOVA) with Bonferroni adjustment). MMC MNs: ***P<0.0001. HMC MNs: ***P<0.0001 and **P=0.001. LMCm MNs: ***P<0.0001 and **P=0.006. LMCl MNs: ***P<0.0001 and *P=0.01. NS, not significant, P>0.5. (d) Quantification of MN percentages at thoracic levels (mean±s.e.m.; n=3 sections averaged per embryo, 3 embryos per genotype; two-way ANOVA with Bonferroni adjustment). HMC MNs: ***P<0.0001. PGC MNs: ***P<0.0001, **P=0.0001 and *P=0.0023. NS, not significant, P>0.5. (e) Quantification of total number of MNs per section (mean±s.e.m.; n=3 sections averaged per embryo, 3 embryos per genotype; two-way ANOVA with Bonferroni adjustment). NS, not significant. P>0.5.