Volume 20 Issue 1, January 2018

Previous work has highlighted the role of metabolic shifts in regulating the formation of memory T cells, which are generated during a primary infection to provide long-lasting immunity. A study now shows that memory T cells rely on a gluconeogenesis–glycogenolysis cycle to provide antioxidant defence and support their survival.

The unfolded protein response (UPR) regulates cell metabolism and survival in response to stress, yet how the UPR is connected to other signalling pathways is poorly understood. PERK is now shown to regulate Bmal1 and Clock proteins to promote cancer cell survival, revealing a link between growth regulation and circadian rhythms.

To overcome the finite supply of muscle stem cells available for cell therapy, a study now describes a strategy for obtaining an unlimited source of myogenic progenitors derived from human pluripotent cells. Two neuronal cell surface receptors facilitate the selection of a population with enhanced regenerative potential.

Friedl and co-authors discuss how migrating cells sense and respond to tissue mechanics, and how cells in turn modify their surroundings.

Glycogen metabolism controls memory T cells. Ma et al. show that the metabolic gene PCK1 promotes glycogen formation, which is used in the pentose phosphate pathway, generating glutathione that is important for counteraction of ROS and thus promotion of memory T-cell maintenance, and resulting in improved antitumour immunity.

Ingallina et al. show that mutant p53 is protected from degradation in response to matrix stiffness in a manner dependent on RhoA geranylgeranylation and actomyosin dynamics.

Takeda et al. reveal that the shortening of epithelial cells required for dorsal fold initiation in Drosophila embryos is driven by a microtubule-based mechanism involving dynein-mediated forces and Katanin-dependent remodelling.

Hicks et al. compare human pluripotent stem cell (hPSC)-derived muscle progenitors to fetal muscle cells, identify ERBB3/NGFR⁺ populations with improved myogenic potential in vivo and enhance cell maturation by inhibiting TGF-β signalling during directed differentiation.

Dziedzic et al. show that the ubiquitin-binding protein ABIN-1 is recruited into TNFR1 signalling complex in a manner dependent on Met1 -ubiquitinating complex LUBAC to regulate K63 de-ubiquitination to activate RIPK1.

Mechanics of epidermal differentiation Miroshnikova et al. find that during embryonic development, epidermal basal layer crowding generates local changes in cell shape, cortical tension, and adhesion that initiate differentiation and delamination

Sato et al. identify ALLO-1 as an autophagy receptor required for paternal organelle clearance in Caenorhabditis elegans, and this process is dependent on ALLO-1 phosphorylation by the TBK1 family kinase IKKE-1.

Chan et al. show that unresolved recombination intermediates form a previously unappreciated type of ultra-fine bridge. These bridges are broken upon cell division, leading to chromosome breaks and instability.

PERK regulates tumour cell survival. Bu et al. show that the unfolded protein response protein PERK induces miR-211 repression of the circadian factor Bmal1 to regulate protein synthesis and stress responses, contributing to tumour progression.