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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Methods Mol Biol. 2017;1622:207–221. doi: 10.1007/978-1-4939-7108-4_15

Figure 3. puf-8/mc6g; lip-1/lip-1; [Pmyo-2::mCherry] transgenic mutants.

Figure 3

(A) Schematic of C. elegans head. (B) Reporter transgenes. puf-8 mutants are maintained using a chromosome II balancer, mc6g, which is marked with Pmyo-2::GFP and dpy-10(e128): puf-8 heterozygotes and lip-1 homozygotes (puf-8/mc6g; lip-1/lip-1; [Pmyo-2::mCherry]) have normal body shape and express both GFP and mCherry (red) in the pharynx and they are fertile (C). puf-8 homozygotes and lip-1 homozygotes (puf-8/puf-8; lip-1/lip-1; [Pmyo-2::mCherry]) have normal body shape and express only mCherry in the pharynx and they are sterile (D). Inhibition of MPK-1/ERK activity by either mpk-1b(RNAi) or U0126 treatment rescues puf-8; lip-1 sterility (E) and their progeny have Pmyo-2::mCherry (Red) fluorescence in the pharynx, which enables effective measuring of the number of viable progeny in wells. Homozygotes for the mc6g balancer also express both GFP and mCherry in the pharynx, but they have an abnormal, dumpy (dpy) body (not shown).