Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Epithelial–mesenchymal transition (EMT) is integral to development and pathology. This switch in cell differentiation and behaviour requires key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix–loop–helix transcription factors, and is regulated by several signalling pathways, including those mediated by the transforming growth factor-β (TGFβ) family.
Intermediate filaments (IFs) are cytoskeletal and nucleoskeletal structures that promote cell integrity and intracellular communication and contribute to subcellular and tissue-specific functions. Our understanding of how post-translational modifications of IF proteins (including nuclear lamins and cytoplasmic keratins, vimentin, desmin, neurofilaments and glial fibrillary acidic protein, among others) regulate IF function is increasing.
The tight regulation of each step of spliceosome assembly from small nuclear RNAs and associated proteins requires coordination between distinct cellular compartments. This in turn dictates where and when alternative splicing occurs and is vital for normal gene expression control.
The eukaryotic 26S proteasome degrades regulatory as well as misfolded or damaged proteins. High-resolution structures of the entire 26S proteasome particle in different nucleotide conditions, and with or without substrate, provide insights into its functional mechanism and will guide genetic and biochemical studies of this key regulatory system.
Engineering of gene circuits, DNA-binding domains and RNA regulators has led to a new generation of synthetic biology research tools, which enable the elucidation of gene function in mammalian cells. The possibility to rebuild complex signalling circuits outside of their normal context is also increasing our understanding of signalling pathways and is leading to innovative therapeutic interventions.
Autophagy and apoptosis control the turnover of organelles and proteins within cells, and of cells within organisms, respectively. It is now clear that these processes often occur sequentially, and that crosstalk between the signalling pathways regulating them generally enables autophagy to block the induction of apoptosis, whereas apoptosis-associated caspase activation shuts off autophagy.
