Two-way feedback between chromatin compaction and histone modification state explains heterochromatin bistability.

Compact chromatin is closely linked with gene silencing in part by sterically masking access to promoters, inhibiting transcription factor binding and preventing polymerase from efficiently transcribing a gene. Here, we propose a broader view: chromatin compaction can be both a cause and a consequence of the histone modification state, and this tight bidirectional interaction can underpin bistable transcriptional states. To test this theory, we developed a mathematical model for the dynamics of the HMR locus in , that incorporates activating histone modifications, silencing proteins and a dynamic, acetylation-dependent, three-dimensional locus size.

Steric interactions and out-of-equilibrium processes control the internal organization of bacteria.

Despite the absence of a membrane-enclosed nucleus, the bacterial DNA is typically condensed into a compact body-the nucleoid. This compaction influences the localization and dynamics of many cellular processes including transcription, translation, and cell division. Here, we develop a model that takes into account steric interactions among the components of the transcriptional-translational machinery (TTM) and out-of-equilibrium effects of messenger RNA (mRNA) transcription, translation, and degradation, to explain many observed features of the nucleoid.

Two timescales control the creation of large protein aggregates in cells.

Protein aggregation is of particular interest because of its connection with many diseases and disorders. Many factors can alter the dynamics and result of this process, one of them being the diffusivity of the monomers and aggregates in the system. Here, we study experimentally and theoretically an aggregation process in cells, and we identify two distinct physical timescales that set the number and size of aggregates.