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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.
Case and Waterman discuss how integrating extracellular-matrix-bound integrins and the actin cytoskeleton into a mechanosensitive molecular clutch transmits actin-cytoskeleton-generated forces to the extracellular matrix through focal adhesions.
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.
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.
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.
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.
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.
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.
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.
Hirano and colleagues have reconstituted mitotic chromatin condensation in cell-free extracts using six purified factors, including histone chaperones, topoisomerase II and condensin I.
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.
Control of stem cell activity is essential for accurate regeneration. Pathogen- or chemical-induced intestinal damage is now shown to recruit haemocytes expressing bone morphogenetic protein signals that stimulate proliferation of intestinal stem cells and subsequently induce their quiescence, in conjunction with muscle-derived bone morphogenetic proteins. A temporal switch in expression of Type I receptors enables this two-phase response.
Cancer cells are known to secrete exosomes with pro-metastatic effects. Pancreatic-cancer-derived exosomes are now shown to promote liver metastasis by eliciting pre-metastatic niche formation through a multi-step process. This involves uptake of exosome-derived factors by liver Kupffer cells and hepatic stellate cell activation to generate a fibrotic microenvironment with immune cell infiltrates that favours metastasis.
A major controversy in the field of chromosome research has been whether condensin is required for achieving the highly compacted state of chromatin fibres in mitosis and meiosis. Through genetic experiments in mouse oocytes, condensin is now found to be indispensable for meiotic chromosome assembly by mediating chromosome compaction and disentanglement of sister chromatids and by conferring rigidity to chromosomes.
Roose and colleagues report that the RasGRP1 and SOS1 guanine nucleotide exchange factors have opposing roles downstream of the EGFR, with RasGRP1 restricting SOS1-induced KRAS-ERK activation and suppressing intestinal tumorigenesis.