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The cell cycle consists of a series of orchestrated events controlled by molecular sensing and feedback networks that ultimately drive the duplication of total DNA and the subsequent division of a single parent cell into two daughter cells. The ability to block the cell cycle and synchronize cells within the same phase has helped understand factors that control cell cycle progression and the properties of each individual phase. Intriguingly, when cells are released from a synchronized state, they do not maintain synchronized cell division and rapidly become asynchronous. The rate and factors that control cellular desynchronization remain largely unknown. In this study, using a combination of experiments and simulations, we investigate the desynchronization properties in cervical cancer cells (HeLa) starting from the G₁/S boundary following double-thymidine block. Propidium iodide (PI) DNA staining was used to perform flow cytometry cell cycle analysis at regular 8 hour intervals, and a custom auto-similarity function to assess the desynchronization and quantify the convergence to an asynchronous state. In parallel, we developed a single-cell phenomenological model the returns the DNA amount across the cell cycle stages and fitted the parameters using experimental data. Simulations of population of cells reveal that the cell cycle desynchronization rate is primarily sensitive to the variability of cell cycle duration within a population. To validate the model prediction, we introduced lipopolysaccharide (LPS) to increase cell cycle noise. Indeed, we observed an increase in cell cycle variability under LPS stimulation in HeLa cells, accompanied with an enhanced rate of cell cycle desynchronization. Our results show that the desynchronization rate of artificially synchronized in-phase cell populations can be used a proxy of the degree of variance in cell cycle periodicity, an underexplored axis in cell cycle research. 

CRISPR-engineered physical unclonable functions establish a foundational security technology for provenance attestation protocols. 

Abstract The ability to detect pathogens specifically and sensitively is critical to combat infectious diseases outbreaks and pandemics. Colorimetric assays involving loop‐mediated isothermal amplification (LAMP) provide simple readouts yet suffer from the intrinsic non‐template amplification. Herein, a highly specific and sensitive assay relying on plasmonic sensing of LAMP amplicons via DNA hybridization, termed as plasmonic LAMP, is developed for the severe acute respiratory syndrome‐related coronavirus 2 (SARS‐CoV‐2) RNA detection. This work has two important advances. First, gold and silver (Au–Ag) alloy nanoshells are developed as plasmonic sensors that have 4‐times stronger extinction in the visible wavelengths and give a 20‐times lower detection limit for oligonucleotides over Au counterparts. Second, the integrated method allows cutting the complex LAMP amplicons into short repeats that are amendable for hybridization with oligonucleotide‐functionalized Au–Ag nanoshells. In the SARS‐CoV‐2 RNA detection, plasmonic LAMP takes ≈75 min assay time, achieves a detection limit of 10 copies per reaction, and eliminates the contamination from non‐template amplification. It also shows better detection specificity and sensitivity over commercially available LAMP kits due to the additional sequence identification. This work opens a new route for LAMP amplicon detection and provides a method for virus testing at its early representation.