Epigenetic signaling and crosstalk in regulation of gene expression and disease progression

Chromatin modifications - including DNA methylation, modification of histones and recruitment of noncoding RNAs - are essential epigenetic events. Multiple sequential modifications converge into a complex epigenetic landscape. For example, promoter DNA methylation is recognized by MeCP2/methyl CpG binding domain proteins which further recruit SETDB1/SUV39 to attain a higher order chromatin structure by propagation of inactive epigenetic marks like H3K9me3. Many studies with new information on different epigenetic modifications and associated factors are available, but clear maps of interconnected pathways are also emerging. This review deals with the salient epigenetic crosstalk mechanisms that cells utilize for different cellular processes and how deregulation or aberrant gene expression leads to disease progression.

Automated summary

Chromatin modifications, such as DNA methylation, histone modification, and recruitment of noncoding RNAs, play essential roles in epigenetic events. These modifications converge into a complex epigenetic landscape, involving the recognition of promoter DNA methylation by MeCP2/methyl CpG binding domain proteins and the recruitment of SETDB1/SUV39 to establish higher order chromatin structure. While many studies have provided new information on different epigenetic modifications and associated factors, clear maps of interconnected pathways are also emerging. This review focuses on the significant crosstalk mechanisms utilized by cells for various cellular processes and how deregulation or aberrant gene expression contributes to disease progression.