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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.
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.
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.
Cell death research was revitalized by the understanding that necrosis can occur in a regulated and genetically controlled manner. Although necroptosis is the most recognized form of regulated necrosis, other examples of this process have emerged. Understanding how these pathways are interconnected should enable regulated necrosis to be therapeutically targeted.