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. Author manuscript; available in PMC: 2013 Apr 10.
Published in final edited form as: Mol Cell Neurosci. 2007 Feb 8;35(1):57–63. doi: 10.1016/j.mcn.2007.02.003

Fig. 5.

Fig. 5

Interaction-deficient FE65 increases average axon segment length but not total neurite or axon length. (A) FE65 mutants that cannot interact with either APP [FE65-mPID2 (mPID2)] or Mena [FE65-mWW (mWW)] (Fig. 1A) decrease the average axon segment length. Axon segment length is assessed by dividing the total axon length (shown in C) by the number of segments per axon (n=30; *p<0.05, **p<0.001). The data shown represent the mean±S.E.M. The data are representative of several such experiments with similar results. (B) The FE65 PID2 mutants illustrated in Fig. 1A do not alter total neurite length. Neurons were infected with adenovirus expressing wild type FE65 (WT), FE65-ΔPID2 (ΔPID2), FE65-mPID2 (mPID2) or GFP virus (CONT) 3 h after plating. Neurites of infected 1 DIV were traced and measured. Total neurite length corresponds to the sum of all segments per process, including the segment extending directly from the soma (see illustration in Fig. 1B). The data are representative of several such experiments with similar results. (C) FE65 mutants do not affect total axon length. Total axon length, the sum of the lengths of all axon segments, was measured in neurons expressing wild type FE65 (WT), FE65-mPID2 (mPID2), FE65-mWW (mWW) or empty virus (CONT).