The human brain transcriptome represents highly organized gene coexpression networks that are consistent across individuals (Hawrylycz et al., 2012; Oldham et al., 2008). Defining gene coexpression patterns for human diseases has revealed convergent molecular profiles (Voineagu et al., 2011), predicted causal systems in neuropathology (Zhang et al., 2013), and unveiled distinct network structures for similar phenotypes (Parikshak et al., 2013). Gene coexpression networks of alcoholic brain tissue, determined with microarray profiling, generated a systemic view of gene expression alterations spanning multiple cell types and brain regions (Ponomarev, Wang, Zhang, Harris, & Mayfield, 2012). A significant portion of transcripts coregulated by chronic alcohol abuse may be conserved within animal models of alcohol consumption (Nunez et al., 2013), permitting an experimentally tractable mode of elucidating gene networks in complex behaviors. Mouse models of alcohol-responsive gene networks can genetically dissect the interrelationship among endophenotypes (Wolen et al., 2012) and clarify networks of candidate genes in alcohol-responsive behaviors (Farris & Miles, 2013). Most network models of acute and chronic alcohol exposure have relied primarily upon microarrays, excluding many available ncRNA substrates. RNA-Seq-derived coexpression networks
