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. 2016 Dec 6;12(12):e1006503. doi: 10.1371/journal.pgen.1006503

Fig 8. Effects of JNK (bsk) overexpression on NP and axon regeneration, and a summary model.

Fig 8

(A) A 48h NP assay was performed in bsk-overexpressing neurons. The green line indicates a stabilized dendrite. Statistical significance was determined by a Fisher’s exact test and the numbers above the bars indicate numbers of neurons analyzed. *** p<0.001. Control data is from Fig 7D. (B) Axon regeneration assays were performed in neurons overexpressing bsk paired with either mCD8-RFP or Nmnat RNAi. UAS-mCD8-RFP was expressed as a control for Nmnat RNAi to keep the number of UAS-controlled transgenes constant and rule out Gal4 dilution effects. Red arrows mark sites of axon injury. The green star indicates the tip of the converted dendrite. Statistical significance was determined by a Mann-Whitney test. Error bars represent SD. *** p<0.001. (C) A summary model of the results is shown. Axon injury activates the DLK/bsk/fos response pathway. The AP-1 transcription factor fos turns on early injury responses that include Nmnat-mediated NP (indicated by darker cell outline in middle image), microtubule dynamics (short green lines in middle image) and mitochondrial fission. NP is mediated by Nmnat, which, if unchecked dampens subsequent regeneration. Caspases and mitochondrial fission counteract NP. (D) Reduction of caspases, increased bsk or fos, or increased Nmnat result in excess or longer than normal NP. Unbalanced NP dampens regeneration.