Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userA transport approach to relate asymmetric protein segregation and population growth
76
0
0.0
(
0
)
Ask ChatGPT about the research
No Arabic abstract
Many unicellular organisms allocate their key proteins asymmetrically between the mother and daughter cells, especially in a stressed environment. A recent theoretical model is able to predict when the asymmetry in segregation of key proteins enhances the population fitness, extrapolating the solution at two limits where the segregation is perfectly asymmetric (asymmetry $a$ = 1) and when the asymmetry is small ($0 leq a ll 1$). We generalize the model by introducing stochasticity and use a transport equation to obtain a self-consistent equation for the population growth rate and the distribution of the amount of key proteins. We provide two ways of solving the self-consistent equation: numerically by updating the solution for the self-consistent equation iteratively and analytically by expanding moments of the distribution. With these more powerful tools, we can extend the previous model by Lin et al. to include stochasticity to the segregation asymmetry. We show the stochastic model is equivalent to the deterministic one with a modified effective asymmetry parameter ($a_{rm eff}$). We discuss the biological implication of our models and compare with other theoretical models.
rate research
Read More
Cancer cell population dynamics often exhibit remarkably replicable, universal laws despite their underlying heterogeneity. Mechanistic explanations of universal cell population growth remain partly unresolved to this day, whereby population feedback between the microscopic and mesoscopic configurations can lead to macroscopic growth laws. We here present a unification under density-dependent birth events via contact inhibition. We consider five classical tumor growth laws: exponential, generalized logistic, Gompertz, radial growth, and fractal growth, which can be seen as manifestations of a single microscopic model. Our theory is substantiated by agent based simulations and can explain growth curve differences in experimental data from in vitro cancer cell population growth. Thus, our framework offers a possible explanation for the large number of mean-field laws that can adequately capture seemingly unrelated cancer or microbial growth dynamics.
In this perspective article, we present a multidisciplinary approach for characterizing protein structure networks. We first place our approach in its historical context and describe the manner in which it synthesizes concepts from quantum chemistry, biology of polymer conformations, matrix mathematics, and percolation theory. We then explicitly provide the method for constructing the protein structure network in terms of non-covalently interacting amino acid side chains and show how a mine of information can be obtained from the graph spectra of these networks. Employing suitable mathematical approaches, such as the use of a weighted, Laplacian matrix to generate the spectra, enables us to develop rigorous methods for network comparison and to identify crucial nodes responsible for the network integrity through a perturbation approach. Our scoring methods have several applications in structural biology that are elusive to conventional methods of analyses. Here, we discuss the instances of: (a) Protein structure comparison that include the details of side chain connectivity, (b) The contribution to node clustering as a function of bound ligand, explaining the global effect of local changes in phenomena such as allostery and (c) The identification of crucial amino acids for structural integrity, derived purely from the spectra of the graph. We demonstrate how our method enables us to obtain valuable information on key proteins involved in cellular functions and diseases such as GPCR and HIV protease, and discuss the biological implications. We then briefly describe how concepts from percolation theory further augment our analyses. In our concluding perspective for future developments, we suggest a further unifying approach to protein structure analyses and a judicious choice of questions to employ our methods for larger, more complex networks, such as metabolic and disease networks.
Many socio-economic and biological processes can be modeled as systems of interacting individuals. The behaviour of such systems can be often described within game-theoretic models. In these lecture notes, we introduce fundamental concepts of evolutionary game theory and review basic properties of deterministic replicator dynamics and stochastic dynamics of finite populations. We discuss stability of equilibria in deterministic dynamics with migration, time-delay, and in stochastic dynamics of well-mixed populations and spatial games with local interactions. We analyze the dependence of the long-run behaviour of a population on various parameters such as the time delay, the noise level, and the size of the population.
We study the dynamics of colonization of a territory by a stochastic population at low immigration pressure. We assume a sufficiently strong Allee effect that introduces, in deterministic theory, a large critical population size for colonization. At low immigration rates, the average pre-colonization population size is small thus invalidating the WKB approximation to the master equation. We circumvent this difficulty by deriving an exact zero-flux solution of the master equation and matching it with an approximate non-zero-flux solution of the pertinent Fokker-Planck equation in a small region around the critical population size. This procedure provides an accurate evaluation of the quasi-stationary probability distribution of population sizes in the pre-colonization state, and of the mean time to colonization, for a wide range of immigration rates. At sufficiently high immigration rates our results agree with WKB results obtained previously. At low immigration rates the results can be very different.
In this work, some phenomenological models, those that are based only on the population information (macroscopic level), are deduced in an intuitive way. These models, as for instance Verhulst, Gompertz and Bertalanffy models, are posted in such a manner that all the parameters involved have physical interpretation. A model based on the interaction (distance dependent) between the individuals (microscopic level) is also presented. This microscopic model reachs the phenomenological models presented as particular cases. In this approach, the Verhulst model represents the situation in which all the individuals interact in the same way, regardless of the distance between them. That means Verhulst model is a kind of mean field model. The other phenomenological models are reaching from the microscopic model according to two quantities: i) the relation between the way that the interaction decays with the distance; and ii) the dimension of the spatial structure formed by the population. This microscopic model allows understanding population growth by first principles, because it predicts that some phenomenological models can be seen as a consequence of the same individual level kind of interaction. In this sense, the microscopic model that will be discussed here paves the way to finding universal patterns that are common to all types of growth, even in systems of very different nature.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
