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. 2008 Dec 5;83(6):752–759. doi: 10.1016/j.ajhg.2008.11.003

Figure 4.

Figure 4

Rescue of slc33a1 Knockdown-Induced Abnormal-Tail Phenotype in Zebrafish by Wild-Type, But Not Mutant, Human SLC33A1 mRNA

(A) Morphological features of zebrafish at 36 hpf from knockdown and rescue experiments. a, Untreated wild-type zebrafish; b, Zebrafish injected with mismatch control MO; c and d, Slc33a1 MO-injected zebrafish with severely curved tail (c) and slightly curved tail (d); e and f, zebrafish coinjected with slc33a1 MO and wild-type human SLC33A1 mRNA—the curly-tail phenotype was rescued completely (e) and partially (f); g and h, zebrafish coinjected with slc33a1 MO and mutated human SLC33A1 mRNA, with severely curved tail (g) or slightly curved tail (h). Scale bar: represents 1 mm.

(B) Phenotype profile from zebrafish knockdown and rescue experiments. The embryos were classified as normal, slightly curly tail, severely curly tail, and lethality, and the percentage for each group is shown.

(C) Defective motor-neuron outgrowth in the reduction of slc33a1. Spinal motor axons were stained with an anti-acetylated tubulin antibody at 36 hr after fertilization. a, motor neurons in spinal cord of zebrafish injected with mismatch control MO; b, injection of slc33a1 MO dramatically impaired outgrowth of motor axons from the spinal cord; c, coinjection of human wild-type SLC33A1 mRNA with slc33a1 MO rescued motor-axon defects; d, Coinjection of mutated human SLC33A1 mRNA did not rescue motor axon defects. Scale bar represents 50 μm.