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. 2024 Dec 3;81(1):478. doi: 10.1007/s00018-024-05523-6

Fig. 5.

Fig. 5

Isl1 continues to regulate TRN identity during late embryogenesis (A-L) In situ hybridization for prethalamic markers on control (SBR-Cre; Isl1F/+) and mutant (SBR-Cre; Isl1F/F) coronal sections at E16.5. Dlx1 expression in the TRN but not in other prethalamic nuclei was lost in Isl1 mutant embryos (G). Meis2 expression, which was restricted to the TRN of control embryos, was abrogated in mutant embryos (H). Loss of Isl1 resulted in ectopic induction of Arx, Pax6, and Lhx1/5 in the TRN (I-L). (M) Quantification of in situ hybridization. The pixel intensity values of TRN or vLG were grouped and averaged from three different sections per embryo (n = 3 embryos; Student’s t-test; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). Scale bars, 200 μm