Figure S3) Modulation of cholinergic signaling via acetylcholine receptors (AChR) does not affect gut morphogenesis. Exposure of X. laevis tadpoles to the AChR agonist carbachol (B) from NF 33-46 does not affect elongation or rotation of the gut relative to water solvent controls (A). Similarly, exposure to the AChR antagonist atropine (D) has no impact on gut morphogenesis relative to DMSO/ethanol treated solvent controls (C). Gut elongation defects observed in AChE-inhibited embryos (e.g., Malathion; E) are not rescued by simultaneously blocking cholinergic signaling with atropine (F). Higher concentrations of carbachol do not affect intestinal development (G), but do result in a significant increase in embryonic lethality (H). Atropine does not rescue intestinal development in AChE inhibited embryos (I), but does reduce Chlorpyrifos-methyl (10mg/L) induced embryonic lethality (J). Neither atropine nor carbachol significantly alter AChE enzymatic activity (K). Scale bars = 1000 um.
Image published in: Pickett MA et al. (2017)
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