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Two studies by Pasakarnis et al. and Ducuing and Vincent show that the actin cable does not drive dorsal closure, but facilitates closure of the epidermis by providing zipping integrity and homogenizing mechanical tension along the leading edge.
Strikoudis et al. show that Phf5a is necessary for ESC self-renewal, efficient iPSC reprogramming and contributes to muscle specification by stabilizing Paf1C and controlling RNA polymerase II elongation.
Bass et al. and Haahr et al. identify ETAA1 as a critical replication stress response factor that interacts with DNA damage response proteins and activates ATR to maintain genomic stability.
In meiosis, double-strand breaks (DSBs) are induced to initiate chromosome pairing and synapsis. Stanzione et al. identify IHO1 as a protein recruited by HORMAD1 to unsynapsed chromosome axes and required for DSB formation.
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.
Muthuswamy et al. report that in macrophages SCRIB interacts with the NADPH oxidase complex to promote the production of reactive oxygen species needed to kill bacteria. Conversely, loss of SCRIB promotes M1 macrophage polarization and inflammation.
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.
Guesdon et al. characterize the microtubule-end-binding region of EB1 using cryo-electron tomography, providing insights into the mechanism of this interaction and the architectural changes in the GTP-cap region during microtubule growth.
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.