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Nuclear dicing bodies were discovered in plants as subcellular droplets of a component of the Dicing complex, which is involved in microRNA production. Now they are revealed to be liquid–liquid phase-separated condensates with intrinsically disordered regions of the Dicing component SERRATE driving both phase separation and miRNA processing.
Xie et al. show that efficient miRNA biogenesis in Arabidopsis requires the assembly of pre-miRNA processing bodies mediated by SERRATE phase separation.
X-chromosome inactivation studies have revealed striking species specificities in terms of the players, kinetics and mechanisms. Transcriptomic profiling of human pre‐implantation development and germ cell differentiation suggests a peculiar dosage compensation mechanism with yet undefined contributions from XIST and XACT lncRNAs.
Chitiashvili et al. report that X-chromosome dosage compensation is achieved via X-chromosome dampening in human female primordial germ cells (hPGCs) and reveal that the lncRNA XACT is a hPGC marker.
Lamm et al. report that replication stress activates mTOR through ATR to induce nuclear actin polymerization, facilitating the recovery from replication stress.
Espanola et al. show in zebrafish that Supt16h, a component of the FACT complex, regulates HSC development through an increase of p53, which promotes expression of phc1, a transcriptional repressor of Notch.
Haltalli et al. show that Plasmodium berghei infection induces interferon release, and affects haematopoietic stem cell proliferation and function, as well as osteoblasts and vascular integrity, in the bone marrow niche.
Luo et al. report that heat stress activates YAP to launch the heat shock transcriptome through inducing dephosphorylation and degradation of LATS independent of the upstream kinases MST and MAP4Ks.
Nguyen et al. show in mouse testes that germ cells are eliminated via apoptosis if they fail to differentiate properly due to errors in epigenetic reprogramming, a process that improves gamete quality.
PI3K–Akt signalling downstream of cell-surface receptor activation has long been thought to occur at the plasma membrane. However, surprising evidence now reveals activation of PI3Kα-mediated PI(3,4,5)P3 synthesis on endosomal membranes that is dependent upon the interaction of PI3Kα with the microtubule-associated protein MAP4.
Intracellularly regulated PI3K activation. Thapa et al. find that phosphatidylinositol-3,4,5-trisphosphate generation and Akt activation occur at intracellular membranes, rather than the plasma membrane, and that this is mediated by MAP4, which controls PI3Kα localization to microtubules.
There are many challenges in finding an effective, long-lasting and universal cure for the whole cohort of patients with Duchenne muscular dystrophy (DMD). The discovery of H19 lncRNA as a stabiliser of dystrophin may prove to be the missing link to the success of various rescue therapies proposed for treating DMD.
Zhang et al. report that the lncRNA H19 stabilizes dystrophin by competing with the ubiquitin E3 ligase TRIM63 for association with dystrophin, thereby alleviating muscular dystrophies.
García-Prat, Perdiguero, Alonso-Martín et al. show that skeletal muscle contains a subpopulation of quiescent stem cells, maintained by FoxO signalling, that is preserved into late life but declines in advanced geriatric age.
Saliakoura et al. find that PLCγ1 is suppressed in hypoxic KRAS-mutant lung cancer cells, which impairs Ca2+ entry into the mitochondria and promotes glycolysis to enhance tumour progression.
Ros et al. show that the ER-resident chaperone calnexin (Cnx) and its partner ERp57 are trafficked to cell surface invadosomes and induce ECM degradation, promoting tumour invasiveness.
Triggering heart repair after myocardial infarction is a challenge in regenerative medicine. A study now shows how ERBB2-mediated YAP activation promotes both cardiomyocyte proliferation and epithelial-to-mesenchymal transition (EMT) in adult mice. EMT initiates cardiomyocyte dedifferentiation and migration and together with proliferation promotes cardiac regeneration.
Aharonov et al. use in vivo genetic approaches to show that ErBB2-mediated YAP activation initiates epithelial–mesenchymal transition-like processes and dedifferentiation of cardiomyocytes to drive heart regeneration.