Utilizing memories properly through forgetting and retrieving is essential for animals to be adapted to changing environment. Yet, its regulatory mechanisms are not fully understood. We previously reported that TIR-1/JNK-1 pathway acts in AWC sensory neurons accelerates forgetting of the olfactory memory in another sensory neurons, AWA. By the Ca2+ imaging analyses, the sensory responses to diacetyl in AWA alter in accordance with the behavioral changes during memory acquisition to forgetting and hence the Ca2+ response can be considered as the sensory memory trace. In this study, by using unbiased genetic screening, we found that mutations result in increased diacylglycerol (DAG) content, such as
dgk-1,
goa-1, or
egl-30 (gf), suppressed the forgetting defect in
tir-1 loss-of-function mutant. However, even though
goa-1;
tir-1 double mutant shows forgetting in chemotaxis like wild-type animals, their Ca2+ responses to diacetyl in AWA did not recover similarly to that in
tir-1 mutant defective in forgetting, suggesting that the sensory memory trace is retained in AWA even though the double mutant exhibits behavioral forgetting. On the contrary, AWC promoter::
goa-1 (gf) expressing mutant showed a forgetting defect in behavior, while it showed recovery in Ca2+ responses. Taken together, proper DAG content in olfactory circuit is important to regulate the switching between forgetting and retrieving of olfactory memories without modifying the sensory memory trace. These results raise two possibilities that inadequate DAG content interferes memory recall, and that, in addition to the sensory memory trace in AWA, memory traces in other neurons are required for the memory recall. We suppose that these two possibilities are not mutually exclusive, and that these are consistent with the mechanisms of the memory retention and recall in mice.