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. Author manuscript; available in PMC: 2015 Jan 16.
Published in final edited form as: Cell Rep. 2013 Dec 27;6(1):93–103. doi: 10.1016/j.celrep.2013.12.004

Figure 5. MEC-17 Acetyltransferase Activity Is Not Required for Axonal Maintenance.

Figure 5

(A) Expression of MEC-17 lacking acetyltransferase activity from the Pmec-4::mec-17(D144N) transgene rescues the axonal degeneration phenotype in ky850, QH4387 (3x outcrossed ky850), and mec-17(ok2109) animals, compared to their nontransgenic siblings.

(B) Expression of the Pmec-4::mec-17(D144N) transgene rescues the mitochondrial distribution defect found in 3-day-old adult mec-17(ok2109) animals, restoring their localization to the WT pattern. MEC-12(K40R) (lacking acetylation residue) animals display a normal distribution of mitochondria.

(C) Quantification of axonal degeneration (L4 stage) in animals carrying single and double mutations in MEC-17 and MEC-12/α-tubulin.

(D) Comparison of axonal degeneration (L4 stage) in mec-17 and mec-7 (encoding β-tubulin) single and double mutants.

(E) Rescue of PLM axonal degeneration in mec-12(e1607) animals with WT MEC-12 or with the MEC-12(K40R) mutated version.

The error bars represent SE of proportion (A and C–E) and SE (B); *p < 0.05; **p < 0.01; ***p < 0.001; n ≥ 100 animals (A and C–E) and ≥24 animals (B).