  Coupling the control of expression stochasticity (noise) to the ability of
expression change (plasticity) can alter gene function and influence
adaptation. A number of factors, such as transcription re-initiation, strong
chromatin regulation or genome neighboring organization, underlie this
coupling. However, these factors do not necessarily combine in equivalent ways
and strengths in all genes. Can we identify then alternative architectures that
modulate in distinct ways the linkage of noise and plasticity? Here we first
show that strong chromatin regulation, commonly viewed as a source of coupling,
can lead to plasticity without noise. The nature of this regulation is relevant
too, with plastic but noiseless genes being subjected to general activators
whereas plastic and noisy genes experience more specific repression.
Contrarily, in genes exhibiting poor transcriptional control, it is
translational efficiency what separates noise from plasticity, a pattern
related to transcript length. This additionally implies that genome neighboring
organization -as modifier- appears only effective in highly plastic genes. In
this class, we confirm bidirectional promoters (bipromoters) as a configuration
capable to reduce coupling by abating noise but also reveal an important
trade-off, since bipromoters also decrease plasticity. This presents ultimately
a paradox between intergenic distances and modulation, with short intergenic
distances both associated and disassociated to noise at different plasticity
levels. Balancing the coupling among different types of expression variability
appears as a potential shaping force of genome regulation and organization.
This is reflected in the use of different control strategies at genes with
different sets of functional constraints.
