GSE208140
Cocaine associated H2AK119ub dynamics in the thalami of Maged1 WT and cKO mice
Maged1 inactivation induces insensitivity to cocaine by impairing cocaine-evoked release of dopamine and plasticity in the Nucleus accumbens (NAc). Here we have characterized the chromatin epigenetic and transcriptional alterations associated with chronic cocaine exposure in the paraventricular thalamus (PVT, one of the main regulatory inputs of the Nac) in mice WT or conditional KO for Maged1 activity. At the epigenetic level, we focused on the analysis of the genomic coverages of the histone post-translational modification H2AK119ub (monoubiquitination of Lysine 119 of H2A; H2Aub), a repressive chromatin mark associated to polycomb (PRC1) –mediated gene repression since Maged1 specifically interact with H2A upon cocaine administration and is required for cocaine-induced increase of H2AK119ub levels in the PVT. Overall design: We dissected the thalami of WT or Maged1 cKO mice after repeated (5) injections of cocaine or saline vehicle, fixed them in 1%PFA and performed ChIPmentation experiments using the anti-i H2AK119ub antibody (Cell Signaling, 8240S). At least 2 independent biological replicates (derived from 3-4 adult mouse thalami each) were processed per each experimental condition.