4,625 research outputs found
Telling time with an intrinsically noisy clock
Intracellular transmission of information via chemical and transcriptional
networks is thwarted by a physical limitation: the finite copy number of the
constituent chemical species introduces unavoidable intrinsic noise. Here we
provide a method for solving for the complete probabilistic description of
intrinsically noisy oscillatory driving. We derive and numerically verify a
number of simple scaling laws. Unlike in the case of measuring a static
quantity, response to an oscillatory driving can exhibit a resonant frequency
which maximizes information transmission. Further, we show that the optimal
regulatory design is dependent on the biophysical constraints (i.e., the
allowed copy number and response time). The resulting phase diagram illustrates
under what conditions threshold regulation outperforms linear regulation.Comment: 10 pages, 5 figure
Optimizing information flow in small genetic networks. II: Feed forward interactions
Central to the functioning of a living cell is its ability to control the
readout or expression of information encoded in the genome. In many cases, a
single transcription factor protein activates or represses the expression of
many genes. As the concentration of the transcription factor varies, the target
genes thus undergo correlated changes, and this redundancy limits the ability
of the cell to transmit information about input signals. We explore how
interactions among the target genes can reduce this redundancy and optimize
information transmission. Our discussion builds on recent work [Tkacik et al,
Phys Rev E 80, 031920 (2009)], and there are connections to much earlier work
on the role of lateral inhibition in enhancing the efficiency of information
transmission in neural circuits; for simplicity we consider here the case where
the interactions have a feed forward structure, with no loops. Even with this
limitation, the networks that optimize information transmission have a
structure reminiscent of the networks found in real biological systems
Control of quantum interference in molecular junctions: Understanding the origin of Fano and anti- resonances
We investigate within a coarse-grained model the conditions leading to the
appearance of Fano resonances or anti-resonances in the conductance spectrum of
a generic molecular junction with a side group (T-junction). By introducing a
simple graphical representation (parabolic diagram), we can easily visualize
the relation between the different electronic parameters determining the
regimes where Fano resonances or anti-resonances in the low-energy conductance
spectrum can be expected. The results obtained within the coarse-grained model
are validated using density-functional based quantum transport calculations in
realistic T-shaped molecular junctions.Comment: 5 pages, 5 figure
Optimizing information flow in small genetic networks. I
In order to survive, reproduce and (in multicellular organisms)
differentiate, cells must control the concentrations of the myriad different
proteins that are encoded in the genome. The precision of this control is
limited by the inevitable randomness of individual molecular events. Here we
explore how cells can maximize their control power in the presence of these
physical limits; formally, we solve the theoretical problem of maximizing the
information transferred from inputs to outputs when the number of available
molecules is held fixed. We start with the simplest version of the problem, in
which a single transcription factor protein controls the readout of one or more
genes by binding to DNA. We further simplify by assuming that this regulatory
network operates in steady state, that the noise is small relative to the
available dynamic range, and that the target genes do not interact. Even in
this simple limit, we find a surprisingly rich set of optimal solutions.
Importantly, for each locally optimal regulatory network, all parameters are
determined once the physical constraints on the number of available molecules
are specified. Although we are solving an over--simplified version of the
problem facing real cells, we see parallels between the structure of these
optimal solutions and the behavior of actual genetic regulatory networks.
Subsequent papers will discuss more complete versions of the problem
Switch‐1 instability at the active site decouples ATP hydrolysis from force generation in myosin II
Myosin active site elements (i.e., switch-1) bind both ATP and a divalent metal to coordinate ATP hydrolysis. ATP hydrolysis at the active site is linked via allosteric communication to the actin polymer binding site and lever arm movement, thus coupling the free energy of ATP hydrolysis to force generation. How active site motifs are functionally linked to actin binding and the power stroke is still poorly understood. We hypothesize that destabilizing switch-1 movement at the active site will negatively affect the tight coupling of the ATPase catalytic cycle to force production. Using a metal-switch system, we tested the effect of interfering with switch-1 coordination of the divalent metal cofactor on force generation. We found that while ATPase activity increased, motility was inhibited. Our results demonstrate that a single atom change that affects the switch-1 interaction with the divalent metal directly affects actin binding and productive force generation. Even slight modification of the switch-1 divalent metal coordination can decouple ATP hydrolysis from motility. Switch-1 movement is therefore critical for both structural communication with the actin binding site, as well as coupling the energy of ATP hydrolysis to force generation
Entanglement and Tensor Product Decomposition for Two Fermions
The problem of the choice of tensor product decomposition in a system of two
fermions with the help of Bogoliubov transformations of creation and
annihilation operators is discussed. The set of physical states of the
composite system is restricted by the superselection rule forbidding the
superposition of fermions and bosons. It is shown that the Wootters concurrence
is not proper entanglement measure in this case. The explicit formula for the
entanglement of formation is found and its dependence on tensor product
decompositions of the Hilbert space is discussed. It is shown that the set of
separable states is narrower than in two-qubit case. Moreover, there exist
states which are separable with respect to all tensor product decompositions of
the Hilbert space.Comment: 8pp, published versio
Destruction of states in quantum mechanics
A description of destruction of states on the grounds of quantum mechanics
rather than quantum field theory is proposed. Several kinds of maps called
supertraces are defined and used to describe the destruction procedure. The
introduced algorithm can be treated as a supplement to the von Neumann-Lueders
measurement. The discussed formalism may be helpful in a description of EPR
type experiments and in quantum information theory.Comment: 14 pp, 1 eps figure, LaTeX2e using iopart class. Final version, will
be published in J. Phys. A: Math. Ge
The linear ubiquitin chain assembly complex regulates TRAIL-induced gene activation and cell death.
The linear ubiquitin chain assembly complex (LUBAC) is the only known E3 ubiquitin ligase which catalyses the generation of linear ubiquitin linkages de novo LUBAC is a crucial component of various immune receptor signalling pathways. Here, we show that LUBAC forms part of the TRAIL-R-associated complex I as well as of the cytoplasmic TRAIL-induced complex II In both of these complexes, HOIP limits caspase-8 activity and, consequently, apoptosis whilst being itself cleaved in a caspase-8-dependent manner. Yet, by limiting the formation of a RIPK1/RIPK3/MLKL-containing complex, LUBAC also restricts TRAIL-induced necroptosis. We identify RIPK1 and caspase-8 as linearly ubiquitinated targets of LUBAC following TRAIL stimulation. Contrary to its role in preventing TRAIL-induced RIPK1-independent apoptosis, HOIP presence, but not its activity, is required for preventing necroptosis. By promoting recruitment of the IKK complex to complex I, LUBAC also promotes TRAIL-induced activation of NF-κB and, consequently, the production of cytokines, downstream of FADD, caspase-8 and cIAP1/2. Hence, LUBAC controls the TRAIL signalling outcome from complex I and II, two platforms which both trigger cell death and gene activation
- …