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. Author manuscript; available in PMC: 2021 May 4.
Published in final edited form as: Dev Cell. 2020 Apr 16;53(3):358–369.e6. doi: 10.1016/j.devcel.2020.03.015

Figure 4. CED-3 Caspase Targets PMK-1(p38 MAPK) to Promote Development and Limit Expression of Anti-Microbial Peptide.

Figure 4.

(A–C) In vitro cleavage analysis with purified CED-3 caspase identifies D327 of PMK-1 as a CED-3 cleavage site. (A) D327A blocks CED-3 cleavage. (B) DxxD cleavage site (P4–P1) residues in PMK-1. Blue triangle indicates scissile bond between the P1 residue, Asp327 (red D) and the P1′ residue, Glu328. (C) D327Aas well as D327E mutations abolish caspase cleavage. Red asterisk, main cleavage product. Purple asterisk, cleavage-resistant full-length protein. Also see Figure S6 for additional Asp to Ala mutants that do not block cleavage.

(D) ced-3(−) animals and pmk-1(D327E) animals show equivalent developmental delay when treated with vhp-1(RNAi). *Significant, mock (RNAi) versus vhp-1(RNAi), p < 0.001, Mann-Whitney. Median values (thin horizontal bars).

(E and F) The pmk-1(D327E) animals show upregulation of nlp-29p::gfp expression equivalent to ced-3(−) animals. Pseudo-colored images (E) and quantification (F) of nlp-29p::gfp expression. Scale bar, 1mm. *Significant, wt versus ced-3(−) and pmk-1(D327E), p < 0.001, Mann-Whitney. Each dot corresponds to an animal. Mean with standard deviation shown.