TY  - GEN
T1  - Silencing the ASI gustatory neuron pair increases expression of the stress-resistance gene sod-3 in a daf-16 and daf-3 independent manner
AU  - Chisnell, Peter
AU  - Kenyon, Cynthia
DO  - 10.17912/W2W37V
UR  - http://beta.micropublication.org/journals/biology/w2w37v/
AB  - Ablation of the gustatory neuron pair ASI has been shown to extend lifespan, and this lifespan extension requires the function of the transcription factor daf-16/FOXO (Alcedo and Kenyon 2004). Given this relationship, we tested whether silencing the neuron pair ASI with the tetanus toxin light chain (Tetx), as opposed to ablating it, could increase the expression of a well- known DAF-16 target, the stress-resistance gene sod-3 (Furuyama et al. 2000; Honda and Honda 1999). Tetanus toxin disrupts neurotransmission by blocking the release of both small clear-core vesicles and large dense-core vesicles, but should not affect communication via gap junctions (Schiavo et al. 1992; McMahon et al. 1992) . In order to measure the effects on sod-3 expression, we measured GFP fluorescence in animals which expressed a psod-3::GFP construct with or without the addition of GFP::Tetx expressed under the ASI-specific promoter pgpa-4 (see methods; Libina et al. 2003). Animals with silenced ASI showed increased fluorescence in the wild- type background (Figure Panel A, B), as well as in loss of function mutants for the genes daf-16 (Figure Panel C) or daf-3 (Figure Panel D), all with P values <0.0001. This finding was unexpected for the following reasons: both genes are required for the lifespan extension caused by loss of signaling from DAF-7/TGFβ (Shaw et al. 2007), which is only secreted from ASI under normal laboratory conditions (Meisel et al. 2014), daf-16 is required for the ablation of ASI to extend lifespan (Alcedo and Kenyon 2004), and optogenetic activation of ASI has been shown to decrease the activity of DAF-16 (Artan et al. 2016).
PY  - 2018
JO  - microPublication Biology
ER  -