DRG axon guidance defects in mve mutant embryos. (A) Diagram of DRG projections in an embryonic spinal cord. Gray planes indicate the orientation and location of optical sections shown in B and C. (B) Confocal images of spinal cord explants infected with HSV-tdTomato to visualize DRG projections. Filopodia are observed on growth cones in control, but not mve, embryos (compare growth cones marked by red arrowheads in ii and iii). (C) Confocal micrographs of whole-mount embryos stained with neurofilament antibody to label axons. Only the right half of the spinal cord is shown for clarity. Boxed areas in i and ii are enlarged in iii and iv. OBH is outlined in red dashed lines in C and D. Boxed region in vi is enlarged in vii, revealing a growth cone lacking filopodia near the ventral midline. (D) Schema of axonal projection patterns observed in control and mve embryos at E10.5 and E12.5. (E) Quantification of central projection defects in wild-type (m+/+v+/+e+/+), littermate ((m+/+v−/−e−/−)/(m+/−v−/−e−/−)), and Ena/VASP null (m−/−v−/−e−/−) embryos. Thoracic spinal levels in six embryos (corresponding to 156 DRG) were scored for each condition; a spinal level was scored as defective if no recognizable OBH was present (C, iv) or if NF-positive axons extend past the OBH toward the dorsal midline (C, vi). Bars: (B, i–iii; and C, i–vi) 50 µm; (C, vii) 10 µm. GAP43, growth associated protein 43; NF, neurofilament; DIV, days in vitro; WT, wild type. Circular objects in C are autofluorescent cells.