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Fig. 3. A catalytically inactive form of human DNMT1 can restore repression and rescue xDMO morphants. (A) Functional domains present in human DNMT1 and an inactivating point mutation of hDNMT1 (hDNMT1^C1226Y) (Jair et al., 2006). (B) Catalytic function of human DNMT1 is not required to rescue xOct25 and xBF2 gene repression. Compare rescue in situ intensities (iii and iv) with signals in control (i) and xDMO morphants (ii). Animal pole views are shown. (C) hDNMT1WT and hDNMT1^C1226Y restore normal Xenopus neurulation with comparable efficiency. Experiment 1 (n=100) is in red and experiment 2 (n=60) is in blue. Compare number of normally neurulating embryos in xDMO only (20%) with rescued injected embryos (>40%). (D) Rescued embryos are similar in phenotype to wild-type siblings. Neurulating embryos are shown. There are apoptotic cells and open blastopores (white arrowheads) in xDMO embryos (bottom left). Such lesions are absent in rescued embryos (right panels), which are similar to control injected embryos (top left) (black arrows indicate neural folds). (E) Phenotypes of late stage (stage 27) embryos. Only 2% (i.e. 98% of embryos fail) of xDMO morphants develop to late tadpole stage (stage 27) compared with 35% and 30% for wild-type (hDNMT1WT) and mutant (hDNMT1^C1226Y) rescued embryos, which develop normally. Scale bars: 1 mm.

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