Abstract

The transmission of changes in phenotype from the parental generation to their offspring after experiencing environmental stress is termed transgenerational memory. Trans-generational epigenetic inheritance (TEI), which involves DNA modification, histone modification, and miRNAs, is the cause of trans-generational memory. This is because they can regulate the expression of genes and relative phenotypes downstream. This article explores the mechanisms under trans-generational memory of an increase in acetophenone sensitivity in mice after the training of odor fear conditioning in the P0 generation. We designed a series of experiments to detect the demethylation status in olfactory sensory neurons (OSNs) and their precursor cells and an artificial edition of the demethylation status by CRISPR d-Cas9 system in either olfactory sensory neuron and sperms. We aim to gain some insights into whether the artificial demethylation of olfactory sensory neurons is sufficient to cause demethylation in sperms (from somatic to germ cells) and whether the artificial demethylation in sperms could lead to demethylation in OSNs in the following generations (from germ cells to somatic cells).

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