Frequency filtering in disordered granular chains

The study of disorder-induced frequency filtering is presented for one-dimensional systems composed of random, pre-stressed masses interacting through both linear and nonlinear (Hertzian) repulsive forces. An ensemble of such systems is driven at a specified frequency, and the spectral content of the propagated disturbance is examined as a function of distance from the source. It is shown that the transmitted signal contains only low-frequency components, and the attenuation is dependent on the magnitude of disorder, the input frequency, and the contact model. It is found that increased disorder leads to a narrower bandwidth of transmitted frequencies at a given distance from the source and that lower input frequencies exhibit less sensitivity to the arrangement of the masses. Comparison of the nonlinear and linear contact models reveals qualitatively similar filtering behavior; however, it is observed that the nonlinear chain produces transmission spectrums with a greater density at the lowest frequencies. In addition, it is shown that random masses sampled from normal, uniform, and binary distributions produce quantitatively indistinguishable filtering behavior, suggesting that knowledge of only the distribution’s first two moments is sufficient to characterize the bulk signal transmission behavior. Finally, we examine the wave number evolution of random chains constrained to move between fixed end-particles and present a transfer matrix theory in wave number space, and an argument for the observed filtering based on the spatial localization of the higher-frequency normal modes

Transcriptional elongation requires DNA break-induced signalling

We have previously shown that RNA polymerase II (Pol II) pause release and transcriptional elongation involve phosphorylation of the factor TRIM28 by the DNA damage response (DDR) kinases ATM and DNA-PK. Here we report a significant role for DNA breaks and DDR signalling in the mechanisms of transcriptional elongation in stimulus-inducible genes in humans. Our data show the enrichment of TRIM28 and γH2AX on serum-induced genes and the important function of DNA-PK for Pol II pause release and transcriptional activation-coupled DDR signalling on these genes. γH2AX accumulation decreases when P-TEFb is inhibited, confirming that DDR signalling results from transcriptional elongation. In addition, transcriptional elongation-coupled DDR signalling involves topoisomerase II because inhibiting this enzyme interferes with Pol II pause release and γH2AX accumulation. Our findings propose that DDR signalling is required for effective Pol II pause release and transcriptional elongation through a novel mechanism involving TRIM28, DNA-PK and topoisomerase II