SUMMARY Gene positioning and regulation of nuclear architecture are thought to influence gene expression. Here, we show that, in mouse olfactory neurons, silent olfactory receptor (OR) genes from different chromosomes converge in a small number of heterochromatic foci. These foci are OR exclusive and form in a cell-type-specific and differentiation-dependent manner. The aggregation of OR genes is developmentally synchronous with the downregulation of lamin b receptor (LBR) and can be reversed by ectopic expression of LBR in mature olfactory neurons. LBR-induced reorganization of nuclear architecture and disruption of OR aggregates perturbs the singularity of OR transcription and disrupts the targeting specificity of the olfactory neurons. Our observations propose spatial sequestering of heterochromatinized OR family members as a basis of monogenic and monoallelic gene expression.

Results of experiments on the dynamics and kinetic roughening of one-dimensional slow-combustion fronts in three grades of paper are reported. Extensive averaging of the data allows a detailed analysis of the spatial and temporal development of the interface fluctuations. The asymptotic scaling properties, on long length and time scales, are well described by the Kardar-Parisi-Zhang ͑KPZ͒ equation with short-range, uncorrelated noise. To obtain a more detailed picture of the strong-coupling fixed point, characteristic of the KPZ universality class, universal amplitude ratios, and the universal coupling constant are computed from the data and found to be in good agreement with theory. Below the spatial and temporal scales at which a crossover takes place to the standard KPZ behavior, the fronts display higher apparent exponents and apparent multiscaling. In this regime the interface velocities are spatially and temporally correlated, and the distribution of the magnitudes of the effective noise has a power-law tail. The relation of the observed short-range behavior and the noise as determined from the local velocity fluctuations is discussed.

The opportunistic pathogen Candida albicans can undergo phenotypic switching between a benign, unicellular phenotype and an invasive, multicellular form that causes candidiasis. Increasingly, strains of Candida are becoming resistant to antifungal drugs, making the treatment of candidiasis difficult, especially in immunocompromised or critically ill patients. Consequently, there is a pressing need to develop new drugs that circumvent fungal drugresistance mechanisms. In this work we used soft X-ray tomography to image the subcellular changes that occur as a consequence of both phenotypic switching and of treating C. albicans with antifungal peptoids, a class of candidate therapeutics unaffected by drug resistance mechanisms. Peptoid treatment suppressed formation of the pathogenic hyphal phenotype and resulted in striking changes in cell and organelle morphology, most dramatically in the nucleus and nucleolus, and in the number, size, and location of lipidic bodies. In particular, peptoid treatment was seen to cause the inclusion of lipidic bodies into the nucleus.

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