18 research outputs found
Goldstone-type fluctuations and their implications for the amorphous solid state
In sufficiently high spatial dimensions, the formation of the amorphous (i.e.
random) solid state of matter, e.g., upon sufficent crosslinking of a
macromolecular fluid, involves particle localization and, concommitantly, the
spontaneous breakdown of the (global, continuous) symmetry of translations.
Correspondingly, the state supports Goldstone-type low energy, long wave-length
fluctuations, the structure and implications of which are identified and
explored from the perspective of an appropriate replica field theory. In terms
of this replica perspective, the lost symmetry is that of relative translations
of the replicas; common translations remain as intact symmetries, reflecting
the statistical homogeneity of the amorphous solid state. What emerges is a
picture of the Goldstone-type fluctuations of the amorphous solid state as
shear deformations of an elastic medium, along with a derivation of the shear
modulus and the elastic free energy of the state. The consequences of these
fluctuations -- which dominate deep inside the amorphous solid state -- for the
order parameter of the amorphous solid state are ascertained and interpreted in
terms of their impact on the statistical distribution of localization lengths,
a central diagnostic of the the state. The correlations of these order
parameter fluctuations are also determined, and are shown to contain
information concerning further diagnostics of the amorphous solid state, such
as spatial correlations in the statistics of the localization characteristics.
Special attention is paid to the properties of the amorphous solid state in two
spatial dimensions, for which it is shown that Goldstone-type fluctuations
destroy particle localization, the order parameter is driven to zero, and
power-law order-parameter correlations hold.Comment: 20 pages, 3 figure
The role of multiple marks in epigenetic silencing and the emergence of a stable bivalent chromatin state
We introduce and analyze a minimal model of epigenetic silencing in budding
yeast, built upon known biomolecular interactions in the system. Doing so, we
identify the epigenetic marks essential for the bistability of epigenetic
states. The model explicitly incorporates two key chromatin marks, namely H4K16
acetylation and H3K79 methylation, and explores whether the presence of
multiple marks lead to a qualitatively different systems behavior. We find that
having both modifications is important for the robustness of epigenetic
silencing. Besides the silenced and transcriptionally active fate of chromatin,
our model leads to a novel state with bivalent (i.e., both active and
silencing) marks under certain perturbations (knock-out mutations, inhibition
or enhancement of enzymatic activity). The bivalent state appears under several
perturbations and is shown to result in patchy silencing. We also show that the
titration effect, owing to a limited supply of silencing proteins, can result
in counter-intuitive responses. The design principles of the silencing system
is systematically investigated and disparate experimental observations are
assessed within a single theoretical framework. Specifically, we discuss the
behavior of Sir protein recruitment, spreading and stability of silenced
regions in commonly-studied mutants (e.g., sas2, dot1) illuminating the
controversial role of Dot1 in the systems biology of yeast silencing.Comment: Supplementary Material, 14 page