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. 2011 Sep 21;6(9):e25047. doi: 10.1371/journal.pone.0025047

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Ezak, Ferkey.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A–D) The OCR-2 NLS is not required for tph-1::gfp expression. (A) TPH-1 is a serotonin biosynthetic enzyme and, as previously described [11], a tph-1p::gfp transcriptional reporter is expressed in the ADF and NSM head neurons. The ADF neurons are indicated. The NSM neurons are seen in the left of each panel. (B) OCR-2 has been reported to modulate transcription of tph-1 [11], and ocr-2(ak47) null mutants have reduced expression of tph-1p::gfp in the ADF neurons. Using the ocr-2 promoter, either (C) the wild-type OCR-2 channel (ocr-2p::ocr-2), or (D) the channel in which the basic residues of the NLS had been mutated to alanine (ocr-2p::ocr-2_NLSmut), was re-introduced into ocr-2(ak47) mutant animals. Both channels restored tph-1p::gfp expression in ADF. (E-H) The OCR-2 NLS is not required for odr-10::gfp expression. ODR-10 is a G protein-coupled receptor and an odr-10p::gfp transcriptional reporter is expressed solely in the AWA head neurons [5]. (E) Expression of odr-10p::gfp in ocr-1(ak46) null mutants is indistinguishable from wild-type animals (and [5]). (F) ocr-2(ak47);ocr-1(ak46) double mutants have drastically reduced expression of odr-10p::gfp (and [5]). Using the ocr-2 promoter, either (G) the wild-type OCR-2 channel (ocr-2p::ocr-2), or (H) the channel in which the basic residues of the NLS had been mutated to alanine (ocr-2p::ocr-2_NLSmut), was re-introduced into ocr-2(ak47);ocr-1(ak46) mutant animals. Both channels restored odr-10p::gfp expression in AWA. ≥2 independent transgenic lines were examined for each construct, n≥40 transgenic animals.