RNA molecules, such as long noncoding RNAs (lncRNAs), have critical roles in regulating gene expression, chromosome architecture, and the modification states of chromatin.
Based on these results, I propose a general, falsifiable theory of individuated multicellularity, which relies on the synergistic coupling across the extracellular space of two explicitly uncorrelated "self-organizing" systems constraining histone modification states at the same sites.
The equilibrium constant between active and inactive states is dependent on these modification states.
Consistent with this view, many remodelling complexes contain components that recognise specific modification states of histone tails.
However, it remains to be determined whether the deubiquiylation process is involved in competition between these two modification states.
These forms could either be the wild type and a truncated form of LYL1 or most likely the wild type LYL1 existing in two post-translational modification states.
In contrast to transcriptional regulation, centromere structure and function is associated both with regulated histone modification states [16], [17] and with rapidly evolving DNA sequences [18], [19], [20].
Among the zebrafish SET domain genes, fifteen maternally expressed ones, which may largely control the programming of histone modification states during very early development, has been identified.
A group of maternal SET domain genes, which are implicated in the programming of histone modification states in early development, have been identified and predicted to be responsible for all known sites of SET domain-mediated histone methylation.
The phenotypes elicited and the context-dependent interplay of the H3-K56 and -S57 point mutations that mimic their respective modification states suggest that serine 57 phosphorylation promotes a nucleosomal transaction when lysine 56 is acetylated.
These combinations represent possible histone modification states at enhancers.
