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Files in this Data Supplement:
Fig. S1. Differentiation of 5HT and motor (VM and SM) neuronal subpopulations in the hindbrain of mutant mice. (A) In Ascl1-null mutants, the downregulation of Insm1 expression is confined to cells in the lateral part of the Nkx2.2-expressing domain (demarcated by square brackets). Insm1 expression is retained in more dorsally located cells in the hindbrain. (B-D) Normal VM and SM neuronal differentiation in Insm1 mutant mice at E12.5. (B) Quantification of the number of Isl1+ cells in the trigeminal and facial nuclei in controls (blue bar) and Insm1 mutants (red bar). (C) Tbx20 expression, and (D) choline acetyltransferase (ChAT) expression (arrowheads) shows that VM differentiation is unperturbed in Insm1 mutants. Lower panels in (C) show that expression of the SM neuronal marker HB9 in neurons of the hypoglossal nucleus (hypog. nuc.) is not altered in Insm1 mutants. (E) Normal neurogenesis (marked by β-tubulin), serotonergic progenitor specification (marked by Foxa2 and Nkx2.2) and absence of cell death in the ventral hindbrain of Insm1 mutants at E11.5 (Foxa2 and Nkx2.2 immunostaining) and E12.5 (β-tubulin and activated Caspase 3 immunostaining).
Fig. S2. Expression of Pet1, Lmx1b and Gata2 in the r1 of control and Insm1 mutant mice at E12.5. Expression was analysed by situ hybridisation. All of these markers are downregulated in the mutants. The square bracket indicates the normal ventral expression of Gata2 that is absent in the equivalent region of Insm1 null mutants (marked by the asterisk).
Fig. S3. Differentiation of central noradrenergic nuclei in Insm1 mutants. (A,B) Expression of various markers, by in situ hybridisation or immunohistochemistry, in the forming LC in E10.5 (A) and E12.5 (B) Insm1 mutants and controls. No difference in expression of Phox2a, Phox2b, DBH or Tlx3 is detectable in Insm1 mutants at E10.5 or E12.5. Quantification of the number of Ascl1+ cells in the dorsal part of r1 at E10.5 (right) does not show any significant difference between Insm1 mutants and controls. (C) Medullary noradrenergic nuclei (A1-2) in Insm1 mutants at E16.5 retain normal expression of Phox2a and DBH. v, IVth ventricle.
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