arXiv subjects

Anna M. C. Andersson

Publications and source records attributed to Anna M. C. Andersson.

3 recordsLinked to original sources

arXiv2008

Efficient Degradation and Expression Prioritization with Small RNAs

We build a simple model for feedback systems involving small RNA (sRNA) molecules based on the iron metabolism system in the bacterium E. coli, and compare it with the corresponding system in H. pylori which uses purely transcriptional regulation. This reveals several unique features of sRNA based regulation that could be exploited by cells. Firstly, we show that sRNA regulation can maintain a smaller turnover of target mRNAs than transcriptional regulation, without sacrificing the speed of response to external shocks. Secondly, we propose that a single sRNA can prioritize the usage of different target mRNAs. This suggests that sRNA regulation would be more common in more complex systems which need to co-regulate many mRNAs efficiently.

q-bio.MN↗

arXiv2006

Genetic Regulation of Fluxes: Iron Homeostasis of Escherichia coli

Iron is an essential trace-element for most organisms. However, because high concentration of free intracellular iron is cytotoxic, cells have developed complex regulatory networks that keep free intracellular iron concentration at optimal range, allowing the incorporation of the metal into iron-using enzymes and minimizing damage to the cell. We built a mathematical model of the network that controls iron uptake and usage in the bacterium Escherichia coli to explore the dynamics of iron flow. We simulate the effect of sudden decrease or increase in the extracellular iron level on intracellular iron distribution. Based on the results of simulations we discuss the possible roles of the small RNA RyhB and the Fe-S cluster assembly systems in the optimal redistribution of iron flows. We suggest that Fe-S cluster assembly is crucial to prevent the accumulation of toxic levels of free intracellular iron when the environment suddenly becomes iron rich.

q-bio.MN↗

arXiv2006

Structure and function of negative feedback loops at the interface of genetic and metabolic networks

The molecular network in an organism consists of transcription/translation regulation, protein-protein interactions/modifications and a metabolic network, together forming a system that allows the cell to respond sensibly to the multiple signal molecules that exist in its environment. A key part of this overall system of molecular regulation is therefore the interface between the genetic and the metabolic network. A motif that occurs very often at this interface is a negative feedback loop used to regulate the level of the signal molecules. In this work we use mathematical models to investigate the steady state and dynamical behaviour of different negative feedback loops. We show, in particular, that feedback loops where the signal molecule does not cause the dissociation of the transcription factor from the DNA respond faster than loops where the molecule acts by sequestering transcription factors off the DNA. We use three examples, the bet, mer and lac systems in E. coli, to illustrate the behaviour of such feedback loops.

q-bio.MN↗