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Fig. 6 Stasimon Is Required for Motor Neuron Development and Rescues SMN-Dependent Motor Axon Defects in Zebrafish Embryos(A) Representative lateral views of motor axons in Tg(mnx1:GFP) zebrafish embryos expressing GFP in motor neurons and injected with control MO, as well as stas MO, smn MO, and tdp43 MO either with or without coinjected human STAS RNA.(B) Quantification of the effects of Stasimon deficiency on motor axon development in zebrafish. Motor axons were scored in Tg(mnx1:GFP) embryos injected with control MO, stas MO, or stas MO + STAS RNA. Embryos were classified as severe, moderate, mild, or no defects based on the severity of motor axon defects, and the percentage for each group is shown.(C) Quantification of Stasimon effects on SMN-dependent motor axon defects in zebrafish. Motor axons were scored in Tg(mnx1:GFP) embryos injected with control MO, smn MO, or smn MO + STAS RNA and embryos were classified as in (B).(D) Quantification of Stasimon effects on TDP43-dependent motor axon defects in zebrafish. Motor axons were scored in Tg(mnx1:GFP) embryos injected with control MO, tdp43 MO, or tdp43 MO + STAS RNA, and embryos were classified as in (B).Data in all graphs are represented as mean and SEM. See also Figure S6.
Reprinted from Cell, 151(2), Lotti, F., Imlach, W.L., Saieva, L., Beck, E.S., Hao le, T., Li, D.K., Jiao, W., Mentis, G.Z., Beattie, C.E., McCabe, B.D., and Pellizzoni, L., An SMN-Dependent U12 Splicing Event Essential for Motor Circuit Function, 440-454, Copyright (2012) with permission from Elsevier. Full text @ Cell