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Using a small-molecule modulator of TORC2 signalling and a mechanosensitive probe, Riggi et al. reveal that decreased plasma membrane tension induces distinct PIP2-enriched domains that sequester and inactivate TORC2.
Castaño et al. show that primary breast tumours drive an IL-1β -mediated inflammatory response that inhibits cellular plasticity and metastatic colonization of metastasis-initiating cells.
Nichols et al. identify an SHP2 inhibitor that disrupts SOS1-mediated RAS–GTP loading with demonstrated efficacy in various types of tumour driven by mutant BRAF, NF1 or RAS.
Lawrence et al. show that mTORC1 capture and activation at the lysosome are regulated by nutrients that destabilize Rag GTPase–Ragulator binding, and delineate how cancer-specific Rag mutants increase mTORC1 signalling.
Almuedo-Castillo et al. show that extirpated embryos are reduced in size but exhibit normal proportions. Following a computational screen, the authors identify an increased concentration of the Nodal inhibitor Lefty to be responsible for the size scaling.
Madaro et al. show that denervation induces accumulation of IL-6–STAT3-activated fibro-adipogenic progenitors without inflammation or muscle regeneration, leading to muscle atrophy and fibrosis.
Massagué and colleagues show that disseminated cancer cells use L1CAM to spread on capillaries and to achieve their outgrowth through activating YAP signalling.
Through CRISPR–Cas9 screen, Dev et al. identified that SHLD1/2 inhibition contributes to PARP-inhibitor resistance. Mechanistically, SHLDs promote non-homologous end-joining and antagonize homologous recombination.
Urra et al. discover that IRE1α, an ER stress mediator, interacts with
filamin A and controls actin dynamics and cell migration in mouse, Drosophila and zebrafish models in a manner independent
of its canonical function.
Using electron and three-dimensional structured illumination microscopy methods, Jana et al. characterize the ciliary base in four different cilia types in Drosophila, discovering structural and protein component differences that may be linked to the diversified functions of cilia.
Bardeesy and colleagues show that mutant GNAS suppresses salt-inducible kinases by activating PKA, leading to lipid remodelling and pancreatic tumourigenesis
Lassard et al. demonstrate a relationship between cellular senescence and perturbed ribosome biogenesis and find that the ribosomal protein S14 is an inhibitor of CDK4, inducing an Rb-dependent cell cycle arrest.
Signalling by the energy sensor kinase AMPK is generally tumour suppressive, but Chhipa et al. show that AMPK is upregulated in glioblastoma, where it phosphorylates CREB1 to enhance HIF1α and GABPA transcription and to support tumour bioenergetics.
Sacristan et al. show that the dynein adaptor Spindly facilitates oligomerisation of the RZZ complex to expand the kinetochore, after which Spindly-associated dynein compacts the kinetochore to allow for faithful chromosome segregation.
Duan et al. find that the membrane skeleton protein spectrin is required for myoblast fusion in Drosophila, accumulating in a mechanosensitive manner in the receiving partner during cell–cell fusion to modulate adhesion and protrusion events.
Reeves et al. use a multistage skin carcinogenesis mouse model and multicoloured lineage tracing to analyse the different patterns of clonal evolution and behaviour seen in progressing and non-progressing papillomas.
Lilja et al. report that multipotent mouse embryonic mammary cells become lineage restricted as early as embryonic day 12.5 during development in a potency switch regulated by Notch1 signalling.
Wuidart et al. show that the mammary gland develops from embryonic multipotent progenitors that switch from multipotency to unipotency and express a unique gene signature. ΔNp63 promotes their basal fate and also reprograms adult luminal cells.
Fang et al. identify a PAX5–OCT4–PRDM1 transcriptional network that acts as a developmental switch in the transition from human pluripotent stem cells to the primordial germ cell lineage.
Pastor et al. demonstrate a role for TFAP2C in the promotion and maintenance of human naive pluripotency by facilitating the opening of enhancers close to pluripotency factors.