EphA7 modulates growth cone morphology yet is dispensable for ephrin-neurotrophin communication.

Hippocampal neurons derived from wild-type (A, C) and EphA7 deficient mice (B, D) were stained for DAPI (blue), tubulin (green) and F-actin (red) expression. Individual growth cones in (A–D) are labeled by an arrow. (A–D) The area of individual growth cones of wild-type neurons (A; higher magnification in C) exceeds that of EphA7 deficient growth cones (B; higher magnification in D). Filopodia length and number was elevated in EphA7 deficient growth cones compared to control. (E) Quantification of growth cone area. Epha7 mutant growth cone area was reduced almost two-fold compared to wild-type. (F) The length of individual filopodia is increased in EphA7 deficient growth cones compared to wild-type. (G, H) The total number of filopodia/growth cone is increased in EphA7 deficient growth cones compared to control (G). (H) depicts the distribution (in percentage) of growth cones harboring a certain filopodia number (1-6 and >6). The frequency of growth cones with 6 or more filopodia is almost doubled upon EphA7 deletion. (I) EphA7 is dispensable for transducing ephrin-A5 collapsing activity in hippocampal neurons. Addition of three concentrations of ephrin-A5 resulted in a comparable growth cone collapse induction in wild-type and EphA7 deficient neurons. (J) EphA7 is not required for ephrin-A mediated suppression of BDNF-evoked growth cone motility. In the absence of EphA7, ephrin-A5 and BDNF co-administration reduced the growth cone area (J), filopodia length and number (data not shown) elevated by BDNF alone. Scale-bar (A, B)  =  10 µm; (C, D)  =  5 µm.