Capacity of a Simple Intercellular Signal Transduction Channel

We model the ligand-receptor molecular communication channel with a discrete-time Markov model, and show how to obtain the capacity of this channel. We show that the capacity-achieving input distribution is iid; further, unusually for a channel with memory, we show that feedback does not increase the capacity of this channel.Comment: 5 pages, 1 figure. To appear in the 2013 IEEE International Symposium on Information Theor

Capacity of a Simple Intercellular Signal Transduction Channel

We model biochemical signal transduction, based on a ligand-receptor binding mechanism, as a discrete-time finite-state Markov channel, which we call the BIND channel. We show how to obtain the capacity of this channel, for the case of binary output, binary channel state, and arbitrary finite input alphabets. We show that the capacity-achieving input distribution is IID. Further, we show that feedback does not increase the capacity of this channel. We show how the capacity of the discrete-time channel approaches the capacity of Kabanov's Poisson channel, in the limit of short time steps and rapid ligand release.Comment: Accepted for publication in IEEE Transactions on Information Theor

Finite-State Channel Models for Signal Transduction in Neural Systems

Information theory provides powerful tools for understanding communication systems. This analysis can be applied to intercellular signal transduction, which is a means of chemical communication among cells and microbes. We discuss how to apply information-theoretic analysis to ligand-receptor systems, which form the signal carrier and receiver in intercellular signal transduction channels. We also discuss the applications of these results to neuroscience.Comment: Accepted for publication in 2016 IEEE International Conference on Acoustics, Speech, and Signal Processing, Shanghai, Chin

Scaling laws for molecular communication

In this paper, we investigate information-theoretic scaling laws, independent from communication strategies, for point-to-point molecular communication, where it sends/receives information-encoded molecules between nanomachines. Since the Shannon capacity for this is still an open problem, we first derive an asymptotic order in a single coordinate, i.e., i) scaling time with constant number of molecules $m$ and ii) scaling molecules with constant time $t$. For a single coordinate case, we show that the asymptotic scaling is logarithmic in either coordinate, i.e., $\Theta(\log t)$ and $\Theta(\log m)$, respectively. We also study asymptotic behavior of scaling in both time and molecules and show that, if molecules and time are proportional to each other, then the asymptotic scaling is linear, i.e., $\Theta(t)=\Theta(m)$.Comment: Accepted for publication in the 2014 IEEE International Symposium on Information Theor

Callose homeostasis at plasmodesmata: molecular regulators and developmental relevance

Plasmodesmata are membrane-lined channels that are located in the plant cell wall and that physically interconnect the cytoplasm and the endoplasmic reticulum (ER) of adjacent cells. Operating as controllable gates, plasmodesmata regulate the symplastic trafficking of micro- and macromolecules, such as endogenous proteins [transcription factors (TFs)] and RNA-based signals (mRNA, siRNA, etc.), hence mediating direct cell-to-cell communication and long distance signaling. Besides this physiological role, plasmodesmata also form gateways through which viral genomes can pass, largely facilitating the pernicious spread of viral infections. Plasmodesmatal trafficking is either passive (e.g., diffusion) or active and responses both to developmental and environmental stimuli. In general, plasmodesmatal conductivity is regulated by the controlled build-up of callose at the plasmodesmatal neck, largely mediated by the antagonistic action of callose synthases (CalSs) and beta-1,3-glucanases. Here, in this theory and hypothesis paper, we outline the importance of callose metabolism in PD SEL control, and highlight the main molecular factors involved. In addition, we also review other proteins that regulate symplastic PD transport, both in a developmental and stress-responsive framework, and discuss on their putative role in the modulation of PD callose turn-over. Finally, we hypothesize on the role of structural sterols in the regulation of (PD) callose deposition and outline putative mechanisms by which this regulation may occur

A role for the extracellular calcium-sensing receptor in cell-cell communication in pancreatic islets of Langerhans

Background: The extracellular calcium-sensing receptor (CaR) is expressed in many tissues that are not associated with Ca2+ homeostasis, including the endocrine cells in pancreatic islets of Langerhans. We have demonstrated previously that pharmacological activation of the CaR stimulates insulin secretion from islet -cells and insulin-secreting MIN6 cells. Methods: In the present study we have investigated the effects of CaR activation on MIN6 cell proliferation and have used shRNA-mediated CaR knockdown to determine whether the CaR is involved in the regulation of insulin secretion via cell-cell communication. Results: CaR activation caused the phosphorylation and activation of the p42/44 MAPK signalling cascade, and this activation was prevented by the shRNA-induced down-regulation of CaR mRNA expression. CaR activation also resulted in increased proliferation of MIN6 cells, consistent with the known role of the p42/44 MAPK system in the regulation of -cell proliferation. Down-regulation of CaR expression had no detectable effects on glucose-induced insulin secretion from MIN6 cells maintained as monolayers, but blocked the increases in insulin secretion that were observed when the cells were configured as three-dimensional islet-like structures (pseudoislets), consistent with a role for the CaR in cell-cell communication in pseudoislets. Conclusion: It is well established that islet function is dependent on communication between islet cells and the results of this study suggest that the CaR is required for -cell to -cell interactions within islet-like structures