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. 2014 Jan 1;28(1):34–43. doi: 10.1101/gad.233643.113

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© 2014 Cochella et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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Figure 5. — die-1 affects antisymmetry of AWC neurons. (A) Expression phenotypes of integrated transgenes of str-2^prom∷GFP(kyIs140), str-2^prom∷TagRFP (vyIs68), and srsx-3^prom∷GFP (vyIs68). (OE) Overexpression. die-1^fosmid∷yfp(OE) data in the sixth and seventh rows are combined from both vyEx1462 and vyEx1476, showing qualitatively similar results. (B,C) Only vyEx1462 was used in double-mutant analysis with unc-36(e251) and sek-1(ag1) and in mosaic analysis. Since the ceh-36 promoter is active in not only AWCL/R but also ASEL/R, we also examined and observed the expected ASER-to-ASEL transformation in ceh-36^prom∷die-1 animals (vyEx1510, 1511) (Supplemental Fig. S3). (B) Expression of an integrated transgene of str-2^prom∷GFP (kyIs140) in die-1(w34) animals with or without the extrachromosomal array die-1^fosmid∷yfp; odr-1^prom∷DsRed (vyEx1462) in total AWC cells. A Z-test was used to calculate P-values. (C) A subset of the data from B is presented here. Shown are only those animals in which die-1 activity is present in one, but not the other, AWC neuron (as assessed with the odr-1^prom∷DsRed array marker), revealing again that die-1 activity correlates with the absence of str-2 expression. A Z-test was used to calculate P-values.