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. Author manuscript; available in PMC: 2016 Feb 15.
Published in final edited form as: Dev Biol. 2014 Dec 16;398(2):255–266. doi: 10.1016/j.ydbio.2014.12.008

Fig. 4. Enhancement of the nekl-3(sv3) phenotype by nekl-2.

Fig. 4

Enhancement of molting defects was assayed in nekl-3(sv3) and nekl-3(gk506) mutant backgrounds. (A-C) Measurements of body length (A), head width (B), and the area of the gonad from a longitudinal section (C) are summarized as box-and-whisker plots (see legend for Fig. 3). A,B, n ≥ 30 for each genotype; C, n ≥ 10. Control RNAi was carried out using strain HT115 carrying vector plasmid pPD129.36. nekl-2(RNAi) enhanced all three aspects of the sv3 mutation but did not affect those of the gk506 mutation. Whereas nekl-1 and nekl-4 RNAi had no effect on either mutation, nekl-3(RNAi) conferred a slight but statistically significant enhancement of gonad defects on sv3 homozygotes. For raw data and statistical analyses (A-C) see Supplementary File 1. (D) Representative images of gonads used for the measurements in C. Gonads of nekl-3(gk506) animals are similar in all RNAi conditions and indicate development to late L1 or early L2. Gonads of nekl-3(sv3) animals typically exhibit more extensive development than that seen for gk506 within the time frame of the experiment and indicate development to mid-to-late L2 stages (sv3 homozygotes can progress to L3 if allowed further growth). RNAi of nekl-2 in the sv3 background leads to L1 or early L2 arrest based on gonad size. Dashed line indicates the gonad periphery. Scale bar = 20 µm.