Page 74 - Q. Neuroscience

[Q. Neuroscience-43]

ascr#3 imprinting is mediated by chromatin remodeling

mechanism

YongJin Cheon¹, Kyuhyung Kim¹

¹Department of Brain and Cognitive Sciences, DGIST, Daegu 42988, Republic of Korea

Early ascaroside#3 pheromone (ascr#3) experience 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 neuron is required for ascr#3 imprinting (Hong et al., 2017). However, circuit and molecular

mechanisms of imprinting need to be further investigated. Here we show that neuronal chromatin remodeling

mechanism plays a critical role for ascr#3 imprinting. We performed candidate gene search and found that ascr#3
imprinting is abolished in set-2 mutants. set-2 encodes a sSET1/MLL histone H3K4 methyltransferase gene and has
been shown to function in germline proliferation (Robert et al., 2014). We also found that ascr#3 imprinting defects

are partially restored upon expression of set-2 cDNA under the control of pan-neuronal promoter. We currently
performing additional rescue experiment. In addition, we will examine odr-2 expression in set-2 mutants.