Imprinting is a form of long-lasting and robust memory which has been described in many animals including human. C. elegans, early experience of ascaroside#3 pheromone (ascr#3, C9, asc-deltaC9) enhances ascr#3 avoidance of adult hermaphrodites via the functional modification of the ascr#3 avoidance circuit. Upregulation of
odr-2 Ly-6-related GPI-linked signaling gene expression in the SMB motor neuron is required for ascr#3 imprinting (Hong et al., 2017). However, circuit and molecular mechanisms underlying imprinting need to be further investigated. Here we show that neuronal chromatin remodeling mechanism may play a critical role for ascr#3 imprinting. We first performed candidate gene search including
set-2 sSET1/MLL histone H3K4 methyltransferase gene. We found that ascr#3 imprinting is abolished in
set-2 mutants. We also found that, whereas expression of
set-2 under the control of own promoter did not rescue imprinting defect of
set-2 mutants, these defects were partially restored upon expression of
set-2 cDNA under the control of pan-neuronal promoter. We are currently performing additional rescue experiment. We are also observing
odr-2 expression level and performing SMB Ca2+ imaging in
set-2 mutant background. This study will allow us to define a common logic for long-lasting memory formation and other forms of behavioral plasticity.