Fig. 9. Model of co-regulation of heterochromatin accessibility by H2A.W and H1.

In WT, H2A.W and H1 both interact with heterochromatin linker DNA to maintain a normal balance of accessibility to chromatin modifiers and DNA methyltransferases in heterochromatin. In the absence of H2A.W, H1 over-accumulates at linker DNA and further reduces accessibility. Loss of H1 alone causes incomplete decompaction, while loss of both H1 and H2A.W causes strong decompaction and increased accessibility. Thus, H2A.W promotes chromatin compaction in the absence of H1, but also promotes heterochromatin ‘breathing’ by opposing excessive H1 incorporation. The thickness of the arrows illustrates the accessibility of MET1, CMT2, CMT3, and DRM2 to DNA. Dashed arrows represent the lowest accessibility, and for solid arrows, the thicker the arrow, the more accessible the heterochromatic DNA.