arXiv subjects

Tao Jia

Publications and source records attributed to Tao Jia.

79 records · Page 5Linked to original sources

arXiv2011

Intrinsic noise in stochastic models of gene expression with molecular memory and bursting

Regulation of intrinsic noise in gene expression is essential for many cellular functions. Correspondingly, there is considerable interest in understanding how different molecular mechanisms of gene expression impact variations in protein levels across a population of cells. In this work, we analyze a stochastic model of bursty gene expression which considers general waiting-time distributions governing arrival and decay of proteins. By mapping the system to models analyzed in queueing theory, we derive analytical expressions for the noise in steady-state protein distributions. The derived results extend previous work by including the effects of arbitrary probability distributions representing the effects of molecular memory and bursting. The analytical expressions obtained provide insight into the role of transcriptional, post-transcriptional and post-translational mechanisms in controlling the noise in gene expression.

q-bio.MN↗

arXiv2010

Measuring Urban Sprawl Based on Massive Street Nodes and the Novel Concept of Natural Cities

In this paper, we develop a novel approach to measuring urban sprawl based on street nodes and naturally defined urban boundaries, both extracted from massive volunteered geographic information OpenStreetMap databases through some data-intensive computing processes. The street nodes are defined as street intersections and ends, while the naturally defined urban boundaries constitute what we call natural cities. We find that the street nodes are significantly correlated with population of cities. Based on this finding, we set street nodes as a proxy of population to measure urban sprawl. We further find that street nodes bear a significant linear relationship with city areal extents. In the plot with the x axis representing city areal extents, and the y axis street nodes, sprawling cities are located below the regression line. We verified the approach using urban areas and population from the US census, and then applied the approach to three European countries: France, Germany, and the United Kingdom for the categorization of natural cities into three classes: sprawling, compact, and normal. This categorization sets a uniform standard for cross comparing sprawling levels across an entire country. Keywords: Street networks, openstreetmap, volunteered geographic information, GIS

physics.data-an↗

arXiv2010

Zipf's Law for All the Natural Cities in the United States: A Geospatial Perspective

This paper provides a new geospatial perspective on whether or not Zipf's law holds for all cities or for the largest cities in the United States using a massive dataset and its computing. A major problem around this issue is how to define cities or city boundaries. Most of the investigations of Zipf's law rely on the demarcations of cities imposed by census data, e.g., metropolitan areas and census-designated places. These demarcations or definitions (of cities) are criticized for being subjective or even arbitrary. Alternative solutions to defining cities are suggested, but they still rely on census data for their definitions. In this paper we demarcate urban agglomerations by clustering street nodes (including intersections and ends), forming what we call natural cities. Based on the demarcation, we found that Zipf's law holds remarkably well for all the natural cities (over 2-4 million in total) across the United States. There is little sensitivity for the holding with respect to the clustering resolution used for demarcating the natural cities. This is a big contrast to urban areas, as defined in the census data, which do not hold stable for Zipf's law. Keywords: Natural cities, power law, data-intensive geospatial computing, scaling of geographic space

physics.data-an↗

arXiv2010

Applications of Little's Law to stochastic models of gene expression

The intrinsic stochasticity of gene expression can lead to large variations in protein levels across a population of cells. To explain this variability, different sources of mRNA fluctuations ('Poisson' and 'Telegraph' processes) have been proposed in stochastic models of gene expression. Both Poisson and Telegraph scenario models explain experimental observations of noise in protein levels in terms of 'bursts' of protein expression. Correspondingly, there is considerable interest in establishing relations between burst and steady-state protein distributions for general stochastic models of gene expression. In this work, we address this issue by considering a mapping between stochastic models of gene expression and problems of interest in queueing theory. By applying a general theorem from queueing theory, Little's Law, we derive exact relations which connect burst and steady-state distribution means for models with arbitrary waiting-time distributions for arrival and degradation of mRNAs and proteins. The derived relations have implications for approaches to quantify the degree of transcriptional bursting and hence to discriminate between different sources of intrinsic noise in gene expression. To illustrate this, we consider a model for regulation of protein expression bursts by small RNAs. For a broad range of parameters, we derive analytical expressions (validated by stochastic simulations) for the mean protein levels as the levels of regulatory small RNAs are varied. The results obtained show that the degree of transcriptional bursting can, in principle, be determined from changes in mean steady-state protein levels for general stochastic models of gene expression.

physics.bio-ph↗

arXiv2010

Post-transcriptional regulation of noise in protein distributions during gene expression

The intrinsic stochasticity of gene expression can lead to large variability of protein levels across a population of cells. Variability (or noise) in protein distributions can be modulated by cellular mechanisms of gene regulation; in particular, there is considerable interest in understanding the role of post-transcriptional regulation. To address this issue, we propose and analyze a stochastic model for post-transcriptional regulation of gene expression. The analytical solution of the model provides insight into the effects of different mechanisms of post-transcriptional regulation on the noise in protein distributions. The results obtained also demonstrate how different sources of intrinsic noise in gene expression can be discriminated based on observations of regulated protein distributions.

q-bio.MN↗

arXiv2010

Agent-based Simulation of Human Movement Shaped by the Underlying Street Structure

Relying on random and purposive moving agents, we simulated human movement in large street networks. We found that aggregate flow, assigned to individual streets, is mainly shaped by the underlying street structure, and that human moving behavior (either random or purposive) has little effect on the aggregate flow. This finding implies that given a street network, the movement patterns generated by purposive walkers (mostly human beings) and by random walkers are the same. Based on the simulation and correlation analysis, we further found that the closeness centrality is not a good indicator for human movement, in contrast to a long standing view held by space syntax researchers. Instead we suggest that Google's PageRank, and its modified version - weighted PageRank, betweenness and degree centralities are all better indicators for predicting aggregate flow.

physics.data-an↗

arXiv2009

Quantifying mRNA synthesis and decay rates using small RNAs

Regulation of mRNA decay is a critical component of global cellular adaptation to changing environments. The corresponding changes in mRNA lifetimes can be coordinated with changes in mRNA transcription rates to fine-tune gene expression. Current approaches for measuring mRNA lifetimes can give rise to secondary effects due to transcription inhibition and require separate experiments to estimate changes in mRNA transcription rates. Here, we propose an approach for simultaneous determination of changes in mRNA transcription rate and lifetime using regulatory small RNAs to control mRNA decay. We analyze a stochastic model for coupled degradation of mRNAs and sRNAs and derive exact results connecting RNA lifetimes and transcription rates to mean abundances. The results obtained show how steady-state measurements of RNA levels can be used to analyze factors and processes regulating changes in mRNA transcription and decay.

q-bio.CB↗