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Fig. 2. Neurogenesis is perturbed in Notch1 conditional mutants at E12.5
when compared with wild-type embryos, but largely recovers by E14.5. (A) The
ganglionic eminences, the LGE and MGE, are drastically reduced in size in
Foxg1Cre; N1 cKOs (asterisks), as seen here in coronal sections
through the forebrain at E12.5. Hes1 and Hes5, genes that
are activated by the Notch signaling pathway, are substantially decreased in
the eye (insets) and telencephalon of Foxg1Cre; N1 cKOs at E12.5.
Mash1, a bHLH gene repressed by Hes activity, is increased in
Foxg1Cre; N1 cKOs at E12.5, particularly in the SVZ (arrows). In
addition, the bHLH gene Neurod is upregulated in the developing
retina (insets). Scale bar: 500 µm. (B) Overall brain morphology and
neurogenesis is relatively normal at E14.5 in Foxg1Cre; N1 cKOs.
Expression of Hes1 and Hes5 appear equivalent in the VZ of
Foxg1Cre; N1 cKOs and wild-type embryos. Unlike at E12.5,
Mash1 is not noticeably upregulated in the SVZ of conditional
knockouts when compared with wild-type embryos at E14.5. Neurogenesis is
further impaired in the retina of Notch1 conditional mutants, as
Hes1 and Hes5 are virtually absent and Neurod is
considerably elevated.
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