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Fig. 7
Pin1 Regulates Sema3A Signaling In Vivo
(A and B) Efficiency of single- and double-morpholino KD of zPin1 and NRP1 in 24-hr zebrafish embryos analyzed by immunoblotting (A), with quantification in (B).
(C) Whole-mount immunostaining of acetylated tubulin in 1-day-old zebrafish embryos demonstrates increased incidence of developmental motor neurons defects, e.g., aberrant branching (arrow) or truncated growth (arrowhead), upon NRP1 KD, which is reduced upon co-injection of Pin1-MO.
(D) Quantification of developmental defects in morpholino-injected zebrafish embryos. Control embryos and Pin1-MO injected do not significantly differ in percentage of defective embryos (17% versus 27%, respectively) or average number of defects per embryo (0.22% versus 0.4%, respectively). NRP1 KD induces defective development in 85% of embryos, with an average of 2.05 defects per embryo. Co-injection of Pin1-MO significantly reduces number of defective embryos (44%) as well as the average number of defects per embryo (0.95).
(E-H) A model of Pin1’s role in Sema3A-driven axonal growth and retraction. Values are means ± SEM.