  Chromatin remodeling machineries are abundant and diverse in eukaryotic
cells. They have been involved in a variety of situations such as histone
exchange and DNA repair, but their importance in gene expression remains
unclear. Although the influence of nucleosome position on the regulation of
gene expression is generally envisioned under the quasi-equilibrium
perspective, it is proposed that given the ATP-dependence of chromatin
remodeling enzymes, certain mechanisms necessitate non-equilibrium treatments.
Examination of the celebrated chromatin remodeling system of the mouse mammary
tumor virus, in which the binding of transcription factors opens the way to
other ones, reveals that breaking equilibrium offers a subtle mode of
transcription factor cooperativity, avoids molecular trapping phenomena and
allows to reconcile previously conflicting experimental data. This mechanism
provides a control lever of promoter responsiveness to transcription factor
combinations, challenging the classical view of the unilateral influence of
pioneer on secondary transcription factors.
