LacI-mediated DNA loops form [7]. Our results imply that an access contribution from environmental fluctuations of only 5% of the ambient thermal temperature T can double the rate at which DNA loops form, which is only a fraction of that which the cytoskeleton can induce upon an embedded polymer [3]. This stochastic mechanism might, therefore, provide an alternate ‘noisy’ means for mechanical control of genetic transcription. Although the rate at which DNA loops form is quite sensitive to environmental fluctua- tions, our data also show that this sensitivity is practically independent of the mean applied tension in the DNA. A separate measurement of the loop formation rate as a function of mean tension, h = 123 , 153 , and 175 fN, collected at a constant applied noise, T$_{α}$/T = 0 . 05, reveals a striking observation: the normalized lifetimes, τ$_{u}$ ( h ; 0 . 05) /τ$_{u}$ ( h ; 0), are constant with an approximate value of 0 . 5 irrespective of the average tension h in the molecule (see Fig. 2). As we will show, this could allow regulatory schemes that are based upon protein- mediated DNA loops to display a significant level of robustness to noise. One might imagine that the increase in looping occurs because the fluctuations allow the random sampling of a low tension regime. However, any increase in looping gained by reducing the tension is negated by the equally likely sampling of high tension fluctuations, requiring us to consider the role of fluctuations in more detail. We begin with an effective FIG. 3: The loop association process can be modeled by diffusion over a barrier. The unlooped lifetime τ$_{u}$ is given by the average time it takes for the DNA to diffuse from the equilibrium position x$_{0}$ , within the energy landscape, to the top of the energy barrier, of magnitude Δ U at x$_{1}$ , where it can escape to infinity and form a loop. 6