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. Author manuscript; available in PMC: 2013 Jul 18.
Published in final edited form as: Science. 2013 Jan 18;339(6117):324–328. doi: 10.1126/science.1231921

Figure 1. Stimulation of Dll1 shedding by GDE2.

Figure 1

(A–H) Coronal sections of E13.5 mouse spinal cords. Arrows mark V2b interneurons (red). (I) Graph quantifying interneuron numbers in WT and Gde2−/− mutants; mean ± s.e.m, n= 4, two-tailed t-test: V0 *p= 0.0016; V1 p= 0.4778; V2a *p= 0.0028, V2b *p= 0.0088 (J) Western blots of extracts of chick spinal cords electroporated with Dll1-Flag plasmid; open arrow = 30kD Dll1 C-terminal fragment, black arrow = C-terminal 42kD Dll1 product (Dll1-42). Arrow (GDE2) = endogenous glycosylated GDE2, lower bands are hypoglycosylated GDE2. (K) Western blot of Jag1 processing (FL= full length; CTF= C-terminal fragment) and quantification of Jag1 CTF/FL ratios from E12.5 embryonic spinal cord extracts. (L–N) Close up of electroporated chick spinal cords (right) shows increased Isl2+ MNs (red) when Dll1 is coelecroporated with GDE2. Arrow = midline. Scale bar = 20µm.