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Sas, M.

Publications and source records attributed to Sas, M..

2 recordsLinked to original sources

Quantifying the Emergence of Population-Level Activity in Neuronal Systems

Collective neural phenomena, such as oscillations and avalanches, are high-level neural signatures observed in aggregated spiking neuronal activity which have been consistently associated with a range of cognitive functions. However, it is often hard to elucidate whether such phenomena are mere epiphenomena or have causal or informational relevance. In this work, we investigate this question by leveraging recent information-theoretic tools to identify emergent phenomena between relevant scales of neural activity. For this, we propose a computational framework combining information-theoretic and network science principles, which we use to investigate emergence in both in-vivo datasets and in-silico simulations. Our approach enables characterisation of emergence phenomena, identifies the relevant scales at which they take place, and elucidates the network-level mechanisms that underpin them. Results show that in-vivo neuronal oscillations show substantial emergent behaviour for smaller prediction delays, while avalanches maintain their emergent nature for larger timescales. These results are supported by in-silico simulations, which show that the emergent signature of oscillations is facilitated by the network structure and interneuronal time-delays. Overall, these results highlight the role of network-level interactions between groups of neuronal assemblies as the key driver of emergent population activity in the brain.

neuroscience↗

Promoter activity buffering reduces the fitness cost of misregulation.

O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY\n\nIn BriefSystematic promoter replacement reveals that coding sequences and 3ends of genes play and active role in buffering cells from fitness defects due to misregulation.\n\nHighlightsO_LIThe TF dose-response curve -- how gene expression changes as a function of TF concentration -- is encoded throughout the gene, not only in the promoter. Genes with the same promoter have different TF DRCs.\nC_LIO_LIA coupled experimental system and mathematical model quantifies the intrinsic ability of genes to buffer or amplify promoter activity.\nC_LIO_LIPromoter activity buffering reduces the effect of misregulation on fitness.\nC_LI\n\nCells regulate gene expression by changing the concentration and activity of transcription factors (TFs). The response of each gene to changes in TF activity is generally assumed to be encoded in the promoter. Here we show that, even when the promoter itself remains constant, each gene has a unique TF dose response curve. Genes have an intrinsic ability to either buffer or amplify the effects of high promoter activity. We present a coupled mathematical model and experimental system for quantifying this property. Promoter activity buffering can be encoded by sequences in both the open reading frame and 3end of genes, and can be implemented by both autoregulatory feedback loops and by titration of limiting trans regulators. We show experimentally that promoter activity buffering insulates cells from fitness defects due to misexpression. The response of genes to changes in [TF] is encoded by sequences outside of the promoter, and this effect can either insulate or amplify the effects of aneuploidy and misregulation on organismal fitness.

systems biology↗