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. Author manuscript; available in PMC: 2016 Jan 15.
Published in final edited form as: Cell. 2015 Jan 15;160(0):161–176. doi: 10.1016/j.cell.2014.11.053

Figure 1. MEKK4 / MLK2 / DLK function as the predominant MAPKKKs in axon degeneration following traumatic injury. See also Figure S3 and Table S1.

Figure 1

(A to C) MEKK4 / MLK2 / DLK regulate degeneration of injured sensory axons. Cultures of embryonic DRG neurons were subjected to lentiviral-shRNA knockdown of MEKK4, MLK2 and DLK, individually or in combination. The efficiency of lentiviral-shRNAs was examined by immunoblot analysis of axonal proteins harvested from each condition (A). Axon degeneration at indicated time points following axotomy was visualized by immunostaining (B), and degeneration was quantified (C), n=3 for each condition. (D and E) MEKK4 / MLK2 / DLK regulate degeneration of injured RGC axons in vivo. RGCs of the mice with indicated genotypes were transduced with TdTomato virus together with either Cre/scrambled-shRNA or Cre/MEKK4-shRNA. Degeneration of TdTomato-positive axons was visualized at indicated time points after optic nerve crush (D), and degeneration was quantified (E), n=4 for each condition. (F and G) MEKK4 / MLK2 / DLK regulate degeneration of injured cortical axons. Cultures of embryonic cortical neurons with indicated genotypes were transduced with lentivirus expressing Cre together with scrambled-shRNA or MEKK4-shRNAs. Axon degeneration at indicated time points following axotomy was visualized by immunostaining (F), and degeneration was quantified (G), n=3 for each condition. Values are presented as mean ± SEM; *, p < 0.01.