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.
Keywords: HIV infection; cancer; constitutive heterochromatin; epigenetic crosstalk; facultative heterochromatin; gene expression.