Coexistence of the superconducting energy gap and pseudogap above and below the transition temperature of superconducting cuprates We express the superconducting gap, ∆(T ), in terms of thermodynamic functions in both s-and d-wave symmetries. Applying to Bi2Sr2CaCu2O 8+δ and Y0.8Ca0.2Ba2Cu3O 7−δ we find that for all dopings ∆(T ) persists, as a partial gap, high above Tc due to strong superconducting fluctuations. Therefore in general two gaps are present above Tc, the superconducting gap and the pseudogap, effectively reconciling two highly polarized views concerning pseudogap physics.

Organisms across all domains of life regulate the size of their cells. However, the means by which this is done is poorly understood. We study two abstracted “molecular” models for size regulation: inhibitor dilution and initiator accumulation. We apply the models to two settings: bacteria like Escherichia coli, that grow fully before they set a division plane and divide into two equally sized cells, and cells that form a bud early in the cell division cycle, confine new growth to that bud, and divide at the connection between that bud and the mother cell, like the budding yeast Saccharomyces cerevisiae. In budding cells, delaying cell division until buds reach the same size as their mother leads to very weak size control, with average cell size and standard deviation of cell size increasing over time and saturating up to 100-fold higher than those values for cells that divide when the bud is still substantially smaller than its mother. In budding yeast, both inhibitor dilution or initiator accumulation models are consistent with the observation that the daughters of diploid cells add a constant volume before they divide. This “adder” behavior has also been observed in bacteria. We find that in bacteria an inhibitor dilution model produces adder correlations that are not robust to noise in the timing of DNA replication initiation or in the timing from initiation of DNA replication to cell division (the C+D period). In contrast, in bacteria an initiator accumulation model yields robust adder correlations in the regime where noise in the timing of DNA replication initiation is much greater than noise in the C + D period, as reported previously (Ho and Amir, 2015). In bacteria, division into two equally sized cells does not broaden the size distribution.

Cells must couple cell-cycle progress to their growth rate to restrict the spread of cell sizes present throughout a population. Linear, rather than exponential, accumulation of Whi5, was proposed to provide this coordination by causing a higher Whi5 concentration in cells born at a smaller size. We tested this model using the inducibleGAL1promoter to make the Whi5 concentration independent of cell size. At an expression level that equalizes the mean cell size with that of wild-type cells, the size distributions of cells with galactose-induced Whi5 expression and wild-type cells are indistinguishable. Fluorescence microscopy confirms that the endogenous andGAL1promoters produce different relationships between Whi5 concentration and cell volume without diminishing size control in the G1 phase. We also expressed Cln3 from the GAL1 promoter, finding that the spread in cell sizes for an asynchronous population is unaffected by this perturbation. Our findings indicate that size control in budding yeast does not fundamentally originate from the linear accumulation of Whi5, contradicting a previous claim and demonstrating the need for further models of cell-cycle regulation to explain how cell size controls passage through Start.

Cells must couple cell cycle progress to their growth rate to restrict the spread of cell sizes present throughout a population. Linear, rather than exponential, accumulation of Whi5, was proposed to provide this coordination by causing a higher Whi5 concentration in cells born at smaller size. We tested this model using the inducible GAL1 promoter to make the Whi5 concentration independent of cell size. At an expression level that equalizes the mean cell size with that of wild-type cells, the size distributions of cells with galactose-induced Whi5 expression and wild-type cells are indistinguishable. Fluorescence microscopy confirms that the endogenous and GAL1 promoters produce different relationships between Whi5 concentration and cell volume without diminishing size control in the G1 phase. We also expressed Cln3 from the GAL1 promoter, finding that the spread in cell sizes for an asynchronous population is unaffected by this perturbation. Our findings contradict the previously proposed model for cell size control in budding yeast and demonstrate the need for a molecular mechanism that explains how cell size controls passage through Start. ClassificationBiological Sciences, Cell Biology. KeywordsWhi5, Start, cell size control, budding yeast, single-cell time-lapse microscopy. Author ContributionsFB performed the experiments, data analysis and simulations. All authors designed the experiments and wrote the manuscript. Significance StatementDespite decades of research, the question of how single cells regulate their size remains unclear. Here we demonstrate that a widely supported molecular model for the fundamental origin of size control in budding yeast is inconsistent with a set of experiments testing the model's key prediction. We therefore conclude that the problem of cell size control in budding yeast remains unsolved. This work highlights the need for rigorous testing of future models of size control in order to make progress on this fundamental question.

Why do large, successful public companies and their CEOs suddenly weaken? To find out, we studied 45 large European and U.S. stumbles. Our case studies point to some common mistakes, such as undertaking unnecessarily risky growth strategies, treating compliance issues lightly, or poor cost control. These simple mistakes often had complex origins, such as attempts to meet conflicting objectives, weak board governance, or even executives being misled by positive experiences with ambitious growth investments. We develop a checklist of “Emperor’s Clothes” failings to help executives and boards lessen the risk of the worst stumbles.