  Recent whole genome polymerase binding assays have shown that a large
proportion of unexpressed genes have pre-assembled RNA pol II transcription
initiation complex stably bound to their promoters. Some such promoter
proximally paused genes are regulated at transcription elongation rather than
at initiation; it has been proposed that this difference allows these genes to
both express faster and achieve more synchronous expression across populations
of cells, thus overcoming molecular "noise" arising from low copy number
factors. It has been established experimentally that genes which are regulated
at elongation tend to express faster and more synchronously; however, it has
not been shown directly whether or not it is the change in the regulated step
{\em per se} that causes this increase in speed and synchrony. We investigate
this question by proposing and analyzing a continuous-time Markov chain model
of polymerase complex assembly regulated at one of two steps: initial
polymerase association with DNA, or release from a paused, transcribing state.
Our analysis demonstrates that, over a wide range of physical parameters,
increased speed and synchrony are functional consequences of elongation
control. Further, we make new predictions about the effect of elongation
regulation on the consistent control of total transcript number between cells,
and identify which elements in the transcription induction pathway are most
sensitive to molecular noise and thus may be most evolutionarily constrained.
Our methods produce symbolic expressions for quantities of interest with
reasonable computational effort and can be used to explore the interplay
between interaction topology and molecular noise in a broader class of
biochemical networks. We provide general-purpose code implementing these
methods.
