|
|
|
|||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
| ||||||||||||||||||||
Files in this Data Supplement:
Fig. S1. Expression of dorsal and ventral telencephalic markers is absent as early as E10-10.5. RNA in situ hybridization of coronal brain sections from E10-10.5 control and FGFR triple mutant embryos. Expression of the telencephalic markers Dlx2 and Emx1 are not detected in the mutant. Arrows point to the telencephalic remnants (dorsal midline, see Fig. 3) in the mutant.
Fig. S2. Expression of Shh appears normal in the FGFR triple mutant at ∼E8.75 by whole-mount RNA in situ hybridization. Arrows point to the anterior limit of forebrain expression.
Fig. S3. Foxg1 expression can at least partially rescue cell death due to the lack of an ANR. (A) Three representative examples of each type of explant: with an ANR (left), without an ANR (middle) and without an ANR but electroporated with a Foxg1-expression construct (right). All explants were electroporated with a GFP-expressing construct. TUNEL staining is in red and Hoechst (blue) was used as a counterstain. (B) Quantification of cell death was done by counting all cells in all sections of at least three explants of each type, excluding cells within ∼25 µm from the edges of the explants.
Fig. S4. Loss of Dlx2 expression in the FGFR double mutants. RNA in situ hybridization of coronal brain sections from E11.5 control and FGFR double mutant embryos. Dlx2 expression is unaffected in the Fgfr2−/−;Fgfr3−/− mutant, appears reduced in the Fgfr1−/−;Fgfr3−/− mutant and is lost in the Fgfr1−/−;Fgfr2−/− mutant. Emx1 expression appears unaffected.
| ||||||||||||||||||||