Third instar larvae expressing ppk11dsRNA.Scer\UAS under the control of Scer\GAL4VGlut-OK371 show no significant increase in quantal content at the neuromuscular junction in the presence of the glutamate receptor antagonist philanthotoxin-433 (10μM), indicating a defect in synaptic homeostasis. In the absence of philanthotoxin-433, the larvae show no significant change in evoked excitatory postsynaptic potential (EPSP) amplitude, miniature mEPSP amplitude or quantal content compared to controls.
Third instar larvae expressing ppk11dsRNA.Scer\UAS under the control of Scer\GAL4Mhc.PW do not show defects in synaptic homeostasis in the presence of philanthotoxin-433.
Larvae expressing ppk11dsRNA.Scer\UAS under the control of Scer\GAL4elav.PLu or Scer\GAL4hs.PB show defective salt-taste behaviour (a reduced preference for 10mM NaCl). The terminal organ of larvae expressing ppk11dsRNA.Scer\UAS under the control of Scer\GAL4elav.PLu shows a reduction in the frequency of action potentials produced in response to salt compared to wild type.
Transcription from the P{UAS-ppk11.dsRNA} construct should produce ppk11 dsRNA, resulting in dsRNA interference (RNAi) of the ppk11 gene.