Systems biology approaches are extensively used to model and reverse engineer gene regulatory networks from experimental data. Conversely, synthetic biology allows "de novo" construction of a regulatory network to seed new functions in the cell. At present, the usefulness and predictive ability of modeling and reverse engineering cannot be assessed and compared rigorously. We built in the yeast Saccharomyces cerevisiae a synthetic network, IRMA, for in vivo "benchmarking" of reverse-engineering and modeling approaches. The network is composed of five genes regulating each other through a variety of regulatory interactions; it is negligibly affected by endogenous genes, and it is responsive to small molecules. We measured time series and steady-state expression data after multiple perturbations. These data were used to assess state-of-the-art modeling and reverse-engineering techniques. A semiquantitative model was able to capture and predict the behavior of the network. Reverse engineering based on differential equations and Bayesian networks correctly inferred regulatory interactions from the experimental data.
Regulations currently in force enable to claim that the lead content in perovskite solar cells is low enough to be safe, or no more dangerous, than other electronics also containing lead. However, the actual environmental impact of lead from perovskite is unknown. Here we show that the lead from perovskite leaking into the ground can enter plants, and consequently the food cycle, ten times more effectively than other lead contaminants already present as the result of the human activities. We further demonstrate that replacing lead with tin represents an environmentally-safer option. Our data suggest that we need to treat the lead from perovskite with exceptional care. In particular, we point out that the safety level for lead content in perovskite-based needs to be lower than other lead-containing electronics. We encourage replacing lead completely with more inert metals to deliver safe perovskite technologies.
Cell identity is determined by specific gene expression patterns that are conveyed by interactions between transcription factors and DNA in the context of chromatin. In development, epigenetic modifiers are thought to stabilize gene expression and ensure that patterns of DNA methylation and histone modification are reinstated in cells as they divide. Global erasure of epigenetic marks occurs naturally at two stages in the mammalian life cycle, but it can also be artificially engineered using a variety of reprogramming strategies. Here we review some of the recent advances in understanding how epigenetic remodeling contributes to conversion of cell fate in vivo and in vitro. We summarize current models of epigenetic erasure and discuss the various enzymes and mechanisms that may operate in cellular reprogramming.
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