Imprecise excision of the Mi{ET1}ppk16MB11536 insertion, resulting in a 767bp deletion that removes two coding exons of ppk16 (a large part of the predicted extracellular domain is removed).
Estimated boundaries of 767 bp deletion resulting from the imprecise excision of Mi{ET1}ppk16MB11536, which removed two exons of ppk16.
Mutant third instar larvae 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, mutant third instar larvae show no significant change in evoked excitatory postsynaptic potential (EPSP) amplitude, an increase in miniature mEPSP amplitude and a decrease in quantal content compared to wild-type controls.
