“…The molecular basis of hybrid incompatibility has been variously attributed to cisor trans-regulatory changes, copy number changes, and amino acid changes (Krüger et al, 2002;Bomblies et al, 2007;Dilkes et al, 2008;, and, thus far, there is little overlap between genes detected in one genus to another (reviewed in Rieseberg and Blackman, 2010). These interactions can affect different targets including pathogen responses (Bomblies et al, 2007;Jeuken et al, 2009;Yamamoto et al, 2010;Mizuno et al, 2011), suppression of transposable elements (TEs) (McClintock, 1984;Shaked et al, 2001;Kashkush et al, 2003;Madlung et al, 2005;Josefsson et al, 2006;Ungerer et al, 2006;Martienssen, 2010), small RNA pathways (Ha et al, 2009;Ng et al, 2012;Shivaprasad et al, 2012;Zhang et al, 2012), and developmental regulatory pathways, such as genomic imprinting in the seed (Josefsson et al, 2006). Importantly, although all these molecular mechanisms have been documented as affected by hybridization in at least one system, their relative contribution to hybrid incompatibility is unclear.…”