While RDE-4 is typically essential for RNAi, we report that in the presence of high concentrations of trigger dsRNA, rde-4 deficient animals are capable of silencing a transgene.
Instead, in the presence of high concentrations of trigger dsRNA, rde-4 animals silence a transgene through an rde-1 dependent mechanism, that by all criteria, corresponds to the canonical RNAi pathway.
These findings suggested that when presented with high concentrations of trigger dsRNA, in this case provided by the GFP[IR] transgene, RDE-4 deficient strains were capable of silencing transgene expression through a process that involved loss of target mRNA, as expected in the canonical RNAi pathway.
Glucose-stimulated insulin release is pulsatile (4, 5), and the pulses reflect coinciding elevations of the concentrations of triggering Ca2+ and amplifying cAMP, which show synchronized oscillations in β-cells (31, 46).
Under optimal conditions, the CL intensity linearly increased with the concentration of the trigger DNA from 0.5 × 10−6 to 1.0 × 10−11 M and the detection limit is 7.0 × 10−12 M.
They observed that increasing concentration of nitrogen triggered higher biomass production.
The lower concentration of taurolidine triggered a greater apoptotic response at both the 12 and 24 hour time points (p < .05).05
We also find that high concentrations of dsRNA trigger lead to increased accumulation of primary siRNAs, consistent with the existence of a rate-limiting step during the conversion of primary to secondary siRNAs.
High concentrations of salt trigger substantial morphological changes to W. ichthyophaga cells.
