Issues

Summary: Abundance and chromatin interactions determine transcription factor function; their disruption can impair development and cause disease. We survey advanced microscopy methodologies that measure these properties and discuss molecular mechanisms that underlie transcription factor haploinsufficiency.

Summary: This Review highlights the physiological relevance of pulmonary neuroendocrine cells, rare airway epithelial cells that form intrapulmonary sensory organs, abnormalities of which are associated with several pulmonary disorders, such as asthma and lung cancer.

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Exploration of the phenotypes associated with the MYH7 R1845W mutation in skeletal muscles, and an alleviating mechanism of the pathological phenotype, suggesting E3-ligase modifier gene activity potentially affects the impact of the mutation.

Summary: We describe a simple murine model of alcoholic hepatitis (AH) to induce injury that recreates many of the key features of AH in human, without the need of challenging surgical procedures to administer ethanol. This will be valuable for testing new therapeutic treatments.

Summary: An assessment of the importance of peri-interventional monitoring to verify a successful experimental performance in order to ensure a disease model that is as homogeneous as possible.

Summary: YY1 contributes to pleuropulmonary blastoma pathogenesis as a downstream target of abnormal epithelial DICER1-cleaved miRNA profile and as a transcriptional regulator of key players of lung development.

Summary: A new non-larval-lethal C. elegans model of spinal muscular atrophy shows mild phenotypes, such as muscle cell and neuronal degeneration, and is therefore useful for testing potential drug treatments.

Summary: We report a 3D quantitative imaging platform (using light-sheet fluorescence microscopy) that can reveal changes in beta cell volume and proliferation, and leukocyte infiltration in pancreata in mouse models of diabetes.

Editor's choice: MYOM2 plays a critical role in establishing or maintaining robust heart function, and is a candidate gene for heart diseases, such as hypertrophic cardiomyopathy and Tetralogy of Fallot.

Summary: The presence of tamoxifen-induced Cre recombinase (merCremer) in the nucleus of cardiomyocytes induces DNA damage and unscheduled cell-cycle activation, indicating the requirement for appropriate controls when using Cre-loxP models for cardiac regeneration studies.