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Fig. 1. Mid/hindbrain phenotype in the absence of total or Gli2A-mediated Shh
signaling. (A-L) Dorsal view of whole-mount brains (A-F), and
Hematoxylin and Eosin staining of midline sagittal sections (G-L) of P0
wild-type (control) and cko embryos or E18.5 null embryos. (B,H) In
Shh-null mutants, cerebral cortex (Ctx), dorsal midbrain (tectum,
Tec), ventral Mb (tegmentum, Teg) and ventral anterior hindbrain (vHb) are not
discernible, and the cerebellum (Cb) is abnormal. (H, inset)
Calbindin-positive Cb Purkinje cells (red, arrow) and Hoechst staining (blue)
of the area indicated by the square. A cell dense layer probably corresponds
to the Cb external granule cells (arrowhead). (C,I) In Smo-En1 cko
mutants, the size of the Mb/Cb is reduced, the ventricle is absent (arrow) and
the Tec is not divided into superior (SC) and inferior colliculi (IC). (D,J)
In Smo-Nes cko mutants, the IC is truncated (arrow) and the Cb is
reduced in size. The Ctx is also reduced in size. (E,F,K,L) In
Gli2-null and Gli2-En1 cko mutants, the Teg, vHb and Cb are
reduced in size. The Tec thins in Gli2-null mutants because of
hydrocephaly. (M-R) Hematoxylin and Eosin staining of midline sagittal
sections of E12.5 wild-type (control) and mutant embryos. (N) In
Shh-null mutants, the mes/r1 is severely reduced in size. Dorsal and
ventral neural tube is joined at the isthmus (Is) (arrow). (O) A close
apposition of ventral and dorsal isthmus (vIs, dIs) is visible in
Smo-En1 cko mutants (arrow), and dorsal mes (d-mes) and r1 (d-r1) are
truncated. (P) In Smo-Nes cko embryos, d-r1 and the posterior d-mes
are reduced in size (arrow), but no obvious defect is observed in ventral mes
(v-mes) or r1 (v-r1). (Q,R) There is no obvious dorsal phenotype in
Gli2-null or Gli2-En1 cko mutants, but ventral mes/r1 is
altered (arrows). Scale bars: 700 µm in A-F; 300 µm in G-L; 75 µm in
M-R.
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