While taxol exposure results in reduced expression of Phsp-6::GFP, Neuro-m-nonN-Nmnat1 (expressed from gcIs41) results in increased expression of Phsp-6::GFP. Taxol treated gcIs41 worms have increased expression not significantly different from gcIs41 alone.
DAF-12 transcription factor binding site in myo-2 promoter was identified by looking for conserved motifs in genes active in the pharynx and then confirming by seeing whether mutation of this motif modulated expession in dauer larvae.
"Surprisingly, in the absence of EtBr, both neuro- and ub-m-nonN-Nmnat1 mildly but significantly increased the basal level of activation of Phsp-6::GFP, and neuro-m-nonN-Nmnat1 increased Phsp-60::GFP (Figures 4c and d)."
DAF-12 transcription factor binding site for ceh-22 was identified by looking for conserved motifs in genes active in the pharynx and then confirming this with gel mobility shift experiments.
DAF-12 transcription factor binding site for ceh-22 was identified by looking for conserved motifs in genes active in the pharynx and then confirming this with gel mobility shift experiments.
"Consistent with the latter hypothesis, taxol dose dependently reduced the basal expression of the Phsp-6::GFP mitoUPR reporter and this reduction of the expression of the mitoUPR reporter was blocked by neuronal m-nonN-Nmnat1 (Figures 5e and f)."
DAF-12 transcription factor binding site in myo-2 promoter was identified by looking for conserved motifs in genes active in the pharynx and then confirming by seeing whether mutation of this motif modulated expession in dauer larvae.
"Surprisingly, in the absence of EtBr, both neuro- and ub-m-nonN-Nmnat1 mildly but significantly increased the basal level of activation of Phsp-6::GFP, and neuro-m-nonN-Nmnat1 increased Phsp-60::GFP (Figures 4c and d)."