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Zhou et al. show that GSK3β phosphorylates KDM1A and induces its deubiquitylation by USP22, leading to demethylation of histone H3K4 and glioblastoma progression.
Weiss and colleagues report that the EMT transcription factors Snail and Slug control skeletal stem cell self-renewal and differentiation by forming transcriptional complexes with the co-activators YAP and TAZ.
It has been unclear how the relatively weak dynein motor can counterbalance kinesin forces during microtubule-dependent transport. Belyy et al. find that binding of dynactin and BICD2 increases the strength of the dynein motor.
Grintsevich et al. discover that the redox enzyme Mical oxidizes F-actin to promote binding of the F-actin-severing protein cofilin, and that the synergy of Mical and cofilin is necessary and sufficient for F-actin disassembly in Drosophila.
Cox et al. report that Yap induces the expression of glutamine synthetase, thereby elevating glutamine and nitrogen levels for de novo nucleotide synthesis. They show that this promotes hepatomegaly and growth of liver cancer cells in zebrafish.
Wickström and colleagues describe how mechanical forces applied to epidermal stem cells lead to relocation of emerin to the nuclear envelope and reduced nuclear actin levels, resulting in chromatin changes that influence lineage commitment.
De Leo et al. identify a lysosomal response to autophagic cargo during lysosome–autophagosome fusion that involves TLR9 activation and OCRL recruitment, and leads to a regulated local increase in PtdIns(4,5)P2, which is necessary for a normal autophagic flux.
Jiang et al. show that Disabled-2 (Dab2) regulates the switch between autophagy and apoptosis in TGB-β-treated cells, through regulation of the Beclin-1–Vps34 interaction.
Walerych et al. show that p53 missense mutants upregulate the proteasome and increase breast cancer cell resistance to proteasome inhibitors. Combined inhibition of p53 mutants and the proteasome leads to increased therapeutic efficacy.
Luschnig and colleagues present a model in which Staccato, in combination with Rab39, mediates the control of apical membrane fusion by interacting with components of the SNARE machinery in the formation of anastomoses in the tracheal tube.
Banh et al. show that PTP1B decreases non-mitochondrial oxygen consumption by regulating the RNF213/α-KGDD pathway, thus promoting hypoxic survival of cancer cells.
Galanos and colleagues observe p21 accumulation in proliferating cancer cells, and show that in cultured p53-null cells, p21 can cause genomic instability by perturbing replication licensing through inhibition of the CRL4-CDT ubiquitin ligase.
Baer et al. report that macrophage-specific DICER deletion abolishes TAM immunosuppressive activity and promotes anti-tumour immunity by recruitment and activation of cytotoxic T cells and increased IFN-γ production.
Kopito and Schrul show that the peroxisome proteins PEX19 and PEX3 mediate the correct insertion of the lipid droplet protein UBXD8 into ER subdomains.
Lee et al. report that aberrantly folded cytosolic proteins are recruited to the ER by the USP19 deubiquitylase, and are then encapsulated in late endosomes that fuse with the plasma membrane, leading to their secretion.
By engineering mice to express a version of the Pten tumour suppressor that lacks the three C-terminal amino acids, van Deursen and colleagues reveal a role for the protein in the generation of symmetric spindles through recruitment of Eg5 to centrosomes.
Torrano et al. use bioinformatics analyses to identify PGC1α as a transcriptional regulator of a metabolic program downstream of ERRα that opposes metastatic dissemination in prostate cancer.
Seokho et al. report that Wnt ligands bind the extracellular domain of polycystin 1 (PKD1) and induce Ca2+ influx through the Ca2+-permeable ion channel TRPP2. This activity is abrogated by PKD1 mutations linked to polycystic kidney disease.
Orhon et al. report that primary-cilium-mediated fluid flow sensing triggers autophagy through LKB1–AMPK–mTOR signalling, and thereby controls the volume of kidney epithelial cells.
Using long-term lineage tracing and mathematical modelling, Tumbar and colleagues define two separate stem cell populations in the epidermis that are regionally clustered, molecularly distinct and show different proliferation dynamics.