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Henninger et al. analyse the early clonal events that underlie haematopoiesis and establish the number of stem cell clones that arise from the ventral dorsal aorta to maintain lifelong blood production.
Anderson et al. show that IQ-motif-containing GTPase-activating protein 1 (IQGAP1) acts as a scaffold for the phosphoinositide kinases that mediate the sequential phosphorylation of phosphoinositides to generate PtdIns(3,4,5)P3 and downstream signalling.
Costa et al. show that asymmetric positioning of the mitotic spindle during endothelial tip cell divisions produces daughter cells of different sizes and the ensuing asymmetry of Vegfr distribution drives Notch-independent tip/stalk cell selection.
Hayer et al. observe that collectively migrating endothelial cells extend rear VE-cadherin-rich membrane structures that are engulfed by follower cells, correlating spatially with the direction of movement.
Caenorhabditis elegans primordial germ cells (PGCs) transiently extend large lobes, which are found to be actively removed and digested by endodermal cells to alter PGC content in a process dependent on actin and dynamin.
Weaver and colleagues report that enrichment of the extracellular matrix with tenascin C promotes aggressiveness of IDH1-mutant glioblastoma by activating a HIF1α-controlled mechanosignalling feedback loop.
Kaminski et al. demonstrate that combined expression of the transcription factors Emx2, Hnf1b, Hnf4a and Pax8 converts mouse and human fibroblasts into induced renal tubular epithelial cells.
Blaas et al. traced Lgr6+ cells during mammary gland formation, homeostasis, pregnancy and tumorigenesis, and found that they represent a population of unipotent progenitors that contribute to alveologenesis and can initiate luminal mammary tumours.
Iwakuma and colleagues report that statins, through their action on the mevalonate pathway, lead to the ubiquitin-mediated degradation of misfolded mutant p53 by impairing its interaction with the Hsp40 family member, DNAJA1.
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.
Fumagalli et al. show that Sec62 delivers ER components to the autolysosome for clearance by acting as a receptor for autophagy protein LC3-II. This identifies Sec62 as a critical factor for selective ER turnover.
Ni et al. report that Snail1 promotes mammary tumour initiation and maintenance independently of its role in EMT. They show that Snail1 forms a complex with HDAC1 and p53 that results in p53 inactivation and degradation, permitting tumour formation.
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.
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.