Transcription-induced active forces suppress chromatin motion by inducing a transient disorder-to-order transition.

Abstract

Recent experiments have shown that the mobility of human interphase chromosome decreases during transcription, and increases upon inhibiting transcription, a finding that is counter-intuitive because it is thought that the active mechanical force ($F$) generated by RNA polymerase II (RNAPII) on chromatin would render it more open and mobile. Inspired by these observations, we use a copolymer model to investigate how $F$ affects the dynamical properties of a single chromatin. The movements of the loci in the gene-rich region are suppressed in an intermediate range of $F$, and are enhanced at small and large $F$ values. In the intermediate $F$, the bond length between consecutive loci increases, becoming commensurate with the location of the minimum in the attractive interaction between the active loci. This results in a transient disorder-to-order transition, leading to the decreased mobility during transcription. Transient ordering of the loci in the gene-rich region might be a mechanism for nucleating a dynamic network involving transcription factors, RNAPII, and chromatin.