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

<p>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. <i>Epha7</i> 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.</p>