FIGURE

Fig. 8

ID

ZDB-FIG-120405-22

Publication

Jao et al., 2012 - A zebrafish model of lethal congenital contracture syndrome 1 reveals Gle1 function in spinal neural precursor survival and motor axon arborization

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Fig. 8

Wild-type human GLE1, but not the Fin_Major mutant form, rescues the defects caused by Gle1 depletion. Embryos from gle1^hi4161a/+ intercrosses were injected with a mix of two non-overlapping gle1 translation-blocking morpholinos (gle1 MOs). Following MO injection, the embryos were injected with buffer alone (gle1 MOs + Buffer) or with <140 pg of in vitro transcribed human GLE1 mRNA (wild type, gle1 MOs + hGLE1_WT; or the Fin_Major mutant form, gle1 MOs + hGLE1_Fin_Major) at the one-cell stage. The extent of head cell death – categorized as severe, mild or wild-type-like (WT-like) – was scored at 32 hpf. Only injecting wild-type GLE1 mRNA, but not the Fin_Major mutant form, rescues the head cell death. At least three independent injections were performed for each condition. Values are mean ± s.e.m. n, number of embryos analyzed in each condition.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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