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dC1GalT1 mutant larvae have also been shown to have morphological defects in the CNS.
Analysis of ATF2 mutant brains has revealed a number of anatomical defects in the CNS.
However, when the p53 MO was co-injected with the ewsr1a MO or the ewsr1b MO, the morphological defect seen in the brain with the ewsr1a or ewsr1b MO alone was rescued, indicating that the morphological defects in the CNS induced by knock-down of ewsr1a and ewsr1b were mediated by the P53 pathway (Figure 5, compare d to e and f to g).
The observed defects in the CNS development would be consistent with elevated apoptosis.
Gars 201R/201R homozygous mutants, however, only survive for a few weeks with major defects in the CNS observed.
Unlike p63, p73 is essential for proper neural development, and p73 knockout mice display developmental defects in the CNS.
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