- Title
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Interaction of survival of motor neuron (SMN) and HuD proteins with mRNA cpg15 rescues motor neuron axonal deficits
- Authors
- Akten, B., Kye, M.J., Hao, L.T., Wertz, M.H., Singh, S., Nie, D., Huang, J., Merianda, T.T., Twiss, J.L., Beattie, C.E., Steen, J.A., and Sahin, M.
- Source
- Full text @ Proc. Natl. Acad. Sci. USA
Cpg15 partially rescues SMN deficiency. (A-C) Lateral-view representative images of Tg(hb9:GFP) embryos at 28 hpf uninjected (A), injected with 9 ng of smn MO (B), and injected with 9 ng of smn MO and 200 ng of full-length human cpg15 mRNA (C). (D) Full-length human cpg15 rescues motor axon defects caused by a reduction of Smn in zebrafish. Tg(hb9:GFP) zebrafish injected with 9 ng of smn MO and scored at 28 hpf using previously published criteria (29) resulted in a distribution of fish with motor nerve defects (n = 260 fish, 5,200 nerves, three injections). Coinjection of 9 ng of smn MO with 200 pg of full-length human cpg15 mRNA was able to partially rescue the nerve defects (n = 326 fish, 6,520 nerves; P < 0.01). The distribution of larval classifications (severe, moderate, mild, and no defects) was analyzed using the Mann–Whitney nonparametric rank test. PHENOTYPE:
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