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Festuccia et al. show that the pluripotency regulator Esrrb is retained on mitotic chromosomes, both in embryonic stem cells and during early embryogenesis, and epigenetically marks key regulatory regions during mitosis.
Bass et al. and Haahr et al. now identify ETAA1 as a critical replication stress response factor that interacts with DNA damage response proteins and activates ATR to maintain genomic stability.
Kodo et al. show that patient-specific iPSC-derived cardiomyocytes recapitulate the proliferative defects associated with the disease, which are a result of TBX20 mutations and abnormal TGF-β signalling.
Johnson et al. report that loss of leukaemia inhibitory factor receptor (LIFR) signalling reduces the expression of genes associated with dormancy in metastatic breast cancer cells, and promotes bone marrow colonization and osteoclastogenesis.
Using a chemical screening approach, Yang and colleagues identify PKC as a regulator of lysosome biogenesis, which controls the subcellular localization of TFEB and ZKSCAN3 through parallel signalling pathways and independently of mTORC1.
Microtubules can self-repair in vitro in response to stress. Théry and colleagues now show that such repair can occur in cells, as free tubulin dimers can be incorporated into a damaged microtubule lattice to promote rescue events.
Pan et al. find that regional glutamine deficiency in melanoma tumours induces tumour cell dedifferentiation and confers therapeutic resistance through histone methylation changes.
Using a chimaeric integrin α5 (where the tail is replaced by that of α2), Yun et al. show that in endothelial cells, integrin α5 interacts with the cAMP-specific phosphodiesterase PDE4D5 to reduce cAMP levels and inflammation both in vitro and in vivo.
Kim et al. demonstrate that sex hormones induce Mib1 expression in myofibres during puberty, initiating the conversion of cycling juvenile satellite cells into adult quiescent satellite cells.
Frede et al. use a chemical carcinogenesis model and lineage tracing to show that oesophageal tumour growth is driven by a single proliferating cancer cell population, suggesting the absence of a hierarchy of proliferating cells in this cancer type.
Dror et al. report that melanoma-derived melanosomes carry miRNAs that induce primary fibroblast reprogramming into cancer-associated fibroblasts, and also induce the formation of a pro-tumorigenic niche.
At sites of cell adhesion to the matrix, integrins are coupled to the actin cytoskeleton through proteins such as talin. Sun et al. now identify Kank2 as an activator of talin that reduces force transmission across focal adhesions.
Cha et al. report that the G9a/RelB axis represses Let-7b through DNMT3A, and sustains K-RAS and β-catenin signalling, thereby controlling the maintenance and function of colorectal-cancer-initiating cells.
Hoare et al. find that NOTCH1 regulates the switch between two distinct senescence-associated secretomes—the TGF-β pathway and pro-inflammatory cytokines—and that its inhibition promotes clearance of oncogene-induced senescent liver cells.
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.
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.