The epigenetic mechanisms, including histone modifications, DNA cytosine methylation, histone variants and noncoding RNAs (ncRNAs), play a key role in determining transcriptional outcomes. Recently, many studies have demonstrated that the different epigenetic mechanisms interplay with each other rather than work independently. In this article, we outline a framework for how different epigenetic mechanisms work with each other in Arabidopsis thaliana.
We build a network of cross-talk between chromatin marks based on six classes of cross-talk interactions. The first pattern details coordinated modifications that act together to enhance or repress gene expression. The second pattern details bivalent modifications that act antagonistically toward gene expression. The third pattern is for unilateral promotion of one modification by the existence of another modification. The fourth pattern is for unilateral inhibition of one modification by another modification. The fifth pattern is for mutual inhibitory patterns. The sixth pattern is for epigenetic modifications that appear independent.
We also explore the mutual regulation between chromatin marks and ncRNAs in various ways. These regulations can be divided into six parts: how ncRNA affects the binding of chromatin mark, such as miR2Epi, siR2Epi and lncR2Epi; how chromatin mark regulates ncRNA, such as Epi2miR, Epi2siR and Epi2lncR.
A comprehensive network of cross-talk between different epigenetic mechanisms will help in fully understanding the functional roles and biological impacts of epigenetic regulation.