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Fig. 2. Neural development defects in mice with targeted disruption of the
Fkbp8 gene. (A) (Top panel) targeting strategy. Black boxes, exons;
arrowheads, PCR primers. (Bottom panels) Left two panels: PCR screening for
targeted ES clones and mouse genotyping. Middle panel: RT-PCR analyses find
the mutant transcripts reduced or absent. E1-3, primers spanning exons 1-3;
E1-7, primers spanning exons 1-7. GAPDH amplification served as a control.
Right panel: immunoblots showing complete ablation of FKBP8 protein.
-tubulin is shown as a gel loading control. (B) Developmental defects
in the CNS of Fkbp8-/- (knockout) embryos. The caudal
neural tube defect (upper left and right) and failure of eye development
(upper right and lower left) are apparent. The mutant neural tube is dilated
(lower right). Dorsal root ganglia (arrowheads) are missing or disorganized.
(C) Apoptosis monitored by immunofluorescence for activated caspase 3.
Sections through the caudal neural tube of E10.5 wild type and
Fkbp8-/- mutant embryos are shown (apoptotic cells are
indicated by white arrows). Quantification (three embryos per genotype and
four sections/embryo) showed no statistically significant difference between
genotypes in the thoracic or lumbar neural tube (NS, not statistically
significant). Scale bars: 100 µm in B; 50 µm in C.
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