ZFIN ID: ZDB-IMAGE-170509-19
Figures for Chitramuthu et al., 2017

Figure Caption/Comments:

Fig. 4

PGRN rescues motor axon defect produced by TDP-43 and FUS knockdown or expression of their mutant mRNAs.

Lateral views (anterior to the left; dorsal to the top) of embryos obtained from the HB9:GFP transgenic fish. Fig 4A. Compared to controls (A1) embryos injected with TDP-43 AMO produced truncated axons (A2). Embryos co-injected with hPGRN mRNA (TDP-43 AMO+hPGRN) partially reversed the truncation phenotype (A3). Fig 4B. Compared to control (B1), embryos injected with FUS AMO produced truncated axons (B2). Embryos co-injected with hPGRN mRNA (FUS AMO +hPGRN) reversed the truncation phenotype (B3). Fig 4C. Compared to controls (C1), embryos injected with TDP43 (G348C) produced truncated axons (C2). Embryos co-injected with hPGRN mRNA (TDP43 (G348C)+hPGRN) reversed the truncation phenotype (C3). Fig 4D. Compared to controls (D1), embryos injected with FUS (R521H) produced truncated axons (D2). Embryos co-injected with hPGRN mRNA (FUS (R521H)+hPGRN) reversed the truncation phenotype (D3). Dashed line indicates the horizontal myoseptum. Arrow points to a single axon. Images were captured at 5X magnification and the hatched box was further subject to 4-5X Zoom.

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