Different promoter affinities account for specificity in MYC-dependent gene regulation

Enhanced expression of the MYC transcription factor is observed in the majority of tumors. Two seemingly conflicting models have been proposed for its function: one proposes that MYC enhances expression of all genes, while the other model suggests gene-specific regulation. Here, we have explored the hypothesis that specific gene expression profiles arise since promoters differ in affinity for MYC and high-affinity promoters are fully occupied by physiological levels of MYC. We determined cellular MYC levels and used RNA- and ChIP-sequencing to correlate promoter occupancy with gene expression at different concentrations of MYC. Mathematical modeling showed that binding affinities for interactions of MYC with DNA and with core promoter-bound factors, such as WDR5, are sufficient to explain promoter occupancies observed in vivo. Importantly, promoter affinity stratifies different biological processes that are regulated by MYC, explaining why tumor-specific MYC levels induce specific gene expression programs and alter defined biological properties of cells

Experiencing the world with archetypal symbols: A new form of aesthetics.

According to the theories of symbolic interactionism, phenomenology of perception and archetypes, we argue that symbols play the key role in translating the information from the physical world to the human experience, and archetypes are the universal knowledge of cognition that generates the background of human experience (the life-world). Therefore, we propose a conceptual framework that depicts how people experience the world with symbols, and how archetypes relate the deepest level of human experience. This framework indicates a new direction of research on memory and emotion, and also suggests that archetypal symbolism can be a new resource of aesthetic experience design.Postprint (published version

A Geometric Fractal Growth Model for Scale Free Networks

We introduce a deterministic model for scale-free networks, whose degree distribution follows a power-law with the exponent $\gamma$. At each time step, each vertex generates its offsprings, whose number is proportional to the degree of that vertex with proportionality constant m-1 (m>1). We consider the two cases: first, each offspring is connected to its parent vertex only, forming a tree structure, and secondly, it is connected to both its parent and grandparent vertices, forming a loop structure. We find that both models exhibit power-law behaviors in their degree distributions with the exponent $\gamma=1+\ln (2m-1)/\ln m$. Thus, by tuning m, the degree exponent can be adjusted in the range, $2 <\gamma < 3$. We also solve analytically a mean shortest-path distance d between two vertices for the tree structure, showing the small-world behavior, that is, $d\sim \ln N/\ln {\bar k}$, where N is system size, and $\bar k$ is the mean degree. Finally, we consider the case that the number of offsprings is the same for all vertices, and find that the degree distribution exhibits an exponential-decay behavior

Constrained spin dynamics description of random walks on hierarchical scale-free networks

We study a random walk problem on the hierarchical network which is a scale-free network grown deterministically. The random walk problem is mapped onto a dynamical Ising spin chain system in one dimension with a nonlocal spin update rule, which allows an analytic approach. We show analytically that the characteristic relaxation time scale grows algebraically with the total number of nodes $N$ as $T \sim N^z$. From a scaling argument, we also show the power-law decay of the autocorrelation function C_{\bfsigma}(t)\sim t^{-\alpha}, which is the probability to find the Ising spins in the initial state {\bfsigma} after $t$ time steps, with the state-dependent non-universal exponent $\alpha$. It turns out that the power-law scaling behavior has its origin in an quasi-ultrametric structure of the configuration space.Comment: 9 pages, 6 figure

Transition from fractal to non-fractal scalings in growing scale-free networks

Real networks can be classified into two categories: fractal networks and non-fractal networks. Here we introduce a unifying model for the two types of networks. Our model network is governed by a parameter $q$. We obtain the topological properties of the network including the degree distribution, average path length, diameter, fractal dimensions, and betweenness centrality distribution, which are controlled by parameter $q$. Interestingly, we show that by adjusting $q$, the networks undergo a transition from fractal to non-fractal scalings, and exhibit a crossover from `large' to small worlds at the same time. Our research may shed some light on understanding the evolution and relationships of fractal and non-fractal networks.Comment: 7 pages, 3 figures, definitive version accepted for publication in EPJ

The influence of gene expression time delays on Gierer-Meinhardt pattern formation systems

There are numerous examples of morphogen gradients controlling long range signalling in developmental and cellular systems. The prospect of two such interacting morphogens instigating long range self-organisation in biological systems via a Turing bifurcation has been explored, postulated, or implicated in the context of numerous developmental processes. However, modelling investigations of cellular systems typically neglect the influence of gene expression on such dynamics, even though transcription and translation are observed to be important in morphogenetic systems. In particular, the influence of gene expression on a large class of Turing bifurcation models, namely those with pure kinetics such as the Gierer–Meinhardt system, is unexplored. Our investigations demonstrate that the behaviour of the Gierer–Meinhardt model profoundly changes on the inclusion of gene expression dynamics and is sensitive to the sub-cellular details of gene expression. Features such as concentration blow up, morphogen oscillations and radical sensitivities to the duration of gene expression are observed and, at best, severely restrict the possible parameter spaces for feasible biological behaviour. These results also indicate that the behaviour of Turing pattern formation systems on the inclusion of gene expression time delays may provide a means of distinguishing between possible forms of interaction kinetics. Finally, this study also emphasises that sub-cellular and gene expression dynamics should not be simply neglected in models of long range biological pattern formation via morphogens