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. Author manuscript; available in PMC: 2010 Mar 4.
Published in final edited form as: Cell. 2009 Sep 4;138(5):1005–1018. doi: 10.1016/j.cell.2009.06.023

Figure 3. rpm-1 and the MAP kinases regulate levels of cebp-1 mRNA via its 3′ UTR.

Figure 3

(A) Quantitative RT-PCR analysis shows up-regulation of cebp-1 mRNA in rpm-1(lf), which is eliminated in dlk-1, pmk-3 or mak-2 mutants (n=3). The control transcript ama-1 encodes the large subunit of RNA polymerase II (Sanford et al., 1983). (B–D) Transgenic expression of mCherry reporters in GABA motor neurons and quantification of fluorescence (n = 35 per genotype). Blue lines and letters denote inclusion of the cebp-1 3′ UTR in the transgene. (B) CEBP-1 with its own 3′ UTR is more highly expressed in rpm-1(lf) and mak-2(EE) transgenic animals than in wild type, dlk-1, and MAK-2(AA) transgenic animals. (C) A CEBP-1 transgene with the unc-54 3′UTR is expressed at similar levels in rpm-1 and wild type. (D) The cebp-1 3′UTR confers up-regulation of mCherry in rpm-1. (E) Expression of cebp-1 with the unc-54 3′UTR causes abnormal motor synapses. Data in A–E shown as mean ± SEM; n = 30 animals per genotype; statistics, Anova. (F) Overexpression of cebp-1 with its own UTR causes PLM axon overextension; transgenes with the unc-54 3′ UTR cause further defects in ALM. Overexpression of cebp-1 from muscles does not affect neuronal morphology. Quantitation, labels, details of mutant phenotypes, promoters and statistics as in Figure 1; GL, # of transgenic lines exhibiting gain-of-function abnormalities. Scales, 10 μm.