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The eukaryotic cell uses two complex machineries to degrade unwanted proteins. The first is the ubiquitin–proteasome system and the second is autophagy. A new study contributes to our understanding of how the two systems interconnect to coordinate protein degradation.
Phagocytic cells engulf their prey into vesicular structures called phagosomes, of which a certain proportion becomes demarcated for enhanced maturation by a process called LC3-associated phagocytosis (LAP). Light has now been shed on the molecular requirements of LAP, establishing a central role for the protein Rubicon in the immune response to Aspergillus fumigatus.
Integrin-based focal adhesions integrate biochemical and biomechanical signals from the extracellular matrix and the actin cytoskeleton. The combination of three-dimensional super-resolution imaging and loss- or gain-of-function protein mutants now links the nanoscale dynamic localization of proteins to their activation and function within focal adhesions.
By measuring surface tensions in developing mouse embryos, Maître and colleagues show that compaction of the blastomere stage embryo is driven by downregulation of actomyosin at cell–cell contacts.
Pei and colleagues report that the oncogene c-Jun acts as a somatic cell reprogramming barrier, and that its truncated dominant-negative form can substitute for Oct4 in reprogramming.
Joglekar and colleagues show that in budding yeast, kinetochore–microtubule attachment mediates silencing of the spindle assembly checkpoint through physical separation of Mps1 kinase from its substrate Spc105.
Waterman and colleagues use super-resolution microscopy and biosensor technology to characterize the spatiotemporal regulation of the protein interactions within focal adhesions that control vinculin activation and function during focal adhesion maturation.
Green and colleagues characterize LC3-associated phagocytosis as a process that depends on Rubicon, Beclin-1, UVRAG and VPS34 but not on canonical autophagy proteins.
Through single-molecule analyses, Brouhard and colleagues find a kinetic barrier to microtubule nucleation, which can be overcome by the action of the microtubule-associated proteins XMAP215 and TPX2.
Kim and colleagues and Kwon and colleagues reveal that amino-terminal arginylation of BiP promotes its targeting to autophagy adaptor p62 and subsequent lysosomal degradation of BiP, p62 and associated cargo.
Williamson and colleagues demonstrate that mRNA-decapping enzyme Dcp2 is phosphorylated by mTORC1, leading to degradation of Atg mRNA and suppression of autophagy, influencing immunity and inflammation.
Tavazoie and colleagues report that activation of pannexin-1 channels and the subsequent stimulation of autocrine purinergic signalling promotes the survival of disseminated cancer cells in the microvasculature of metastasis target organs.
