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. 2016 Aug 31;6(8):160091. doi: 10.1098/rsob.160091

Figure 1.

Figure 1.

Temporal sequence ATF3 induction in injured facial motoneurons. (a–f) FN of wt (a–e) and Atf3 mutant (f) animals were stained for ATF3 expression before (a) or several days post-lesion (d.p.l.; b–f). ATF3 is not present in uninjured FMNs (a) or only weakly at 6 h after lesion (b). By contrast, at 3 (c) and 7 (d) d.p.l., ATF3 was localized to FMNs. After three weeks of lesion, there was almost no ATF3 expression (e). In Atf3 mutant mice, no ATF3 expression was visible at 3 d.p.l. (f). (g) Quantification of the number of ATF3 positive FMNs per section at different times after facial nerve injury. (h) Analysis of Atf3, Atf2, Atf4 and Atf6 mRNA abundance in FNs without and 3 d.p.l. in wt and Atf3 mutant mice. Only Atf3, but no other family member, was induced by facial nerve injury in wt neurons. No compensatory expression of Atf2, Atf4 or Atf6 was observed in Atf3 mutant animals. (i,j) Unlesioned (i) and lesioned (j) facial nerves were stained for ATF3 expression. Without injury (i), no ATF3 expression was observed. By contrast, ATF3 was present in Schwann cells of an injured facial nerve (arrows in j). n ≥ 3 animals each bar. Data are presented as mean ± s.d. ***p ≤ 0.001. Scale bar (a–f) = 100 µm; (i,j) = 50 µm.