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Cancer. Normal mammary stem cells and breast cancer stem cells evade the suppressive effects of macrophage-derived interferon through elevated expression of miR-199a, allowing the preservation of stem cell properties and the acquisition of tumour-initiating abilities.p711
Mechanobiology — the study of how physical forces control the behaviour of cells and tissues — is a rapidly growing field. In this issue, we launch a Series of specially commissioned Review articles that discuss exciting recent developments in this area.
Nature Cell Biology is among the Springer Nature journals taking part in a recently launched trial that mandates the provision of ORCID identifiers for the corresponding authors of our papers.
In this Review, we will discuss how the interplay and feedback between mechanical and biochemical signals control tissue morphogenesis and cell fate specification in embryonic development.
Due to their varied metabolic and signalling roles, mitochondria are important in mediating cell behaviour. By altering mitochondrial function, two studies now identify metabolite-induced epigenetic changes that have profound effects on haematopoietic stem cell fate and function.
Epithelial cells form energetically costly cell–cell adhesions in response to mechanical forces. How cells obtain their energy during this event is unclear. Activity of a key regulator of cell metabolism, the AMP-activated protein kinase (AMPK), is now shown to be mechanoresponsive, and thus can bridge adhesion mechanotransduction and energy homeostasis.
Vascular malformations result from improper blood vessel responses to molecular and mechanical signals. Two studies now show that endothelial cell migration and cell shape changes are perturbed in mutants lacking the TGFβ/BMP co-receptor endoglin, leading to arteriovenous shunts. Endoglin coordinates endothelial cell responses to ligand–receptor signalling and flow-mediated mechanical cues.
The involvement of proliferation and migration in epidermal healing has long been recognized, but three studies now reveal how a variety of individual cell behaviours achieve a collective epithelial response, and how diverse repair routes are taken by cells of different origins.
Little is known regarding how the interactions of stem cells with the immune system regulate their plasticity. A study now describes a mechanism by which normal breast and cancer stem cells utilize miR-199a to downregulate the corepressor LCOR and minimize responses to type I interferon.
Donati et al. show that following skin wounding a differentiated Gata6+ cell population resident in the sebaceous duct migrates to the interfollicular epidermis and reattaches to the basal membrane, dedifferentiating into stem cells.
Two papers by Liu et al. and Ansó et al. study the post-transcriptional regulation of mitochondrial factors in erythropoiesis and the role of RISP-mediated mitochondrial respiration in fetal and adult HSC function via metabolites and epigenetic changes.
Two papers by Liu et al. and Ansó et al. study the post-transcriptional regulation of mitochondrial factors in erythropoiesis and the role of RISP-mediated mitochondrial respiration in fetal and adult HSC function via metabolites and epigenetic changes.
Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls blood vessel diameter in response to blood flow.
Two studies by Sugden et al. and Jin et al. show that endoglin regulates endothelial cell migration through VEGFR2 signalling and controls blood vessel diameter in response to blood flow.
Hoeck et al. show that disruption of the hair follicle stem cell compartment by loss of Lgr5+ stem cells is followed by an inflammatory response and CD34+ stem cell activation and proliferation, to eventually replenish the Lgr5+ population.
Decker et al. show that leptin-receptor-positive mesenchymal stromal cells are the source of the fibrogenic myofibroblasts that expand in primary myelofibrosis in a process mediated by PDGFRA pathway activation.
Cortical tension is thought to be generated by myosin II, and little is known about the role of actin network properties. Chugh et al. demonstrate that actin cortex thickness, determined by actin filament length, influences cortical tension.
Tavernier et al. show that loss of the protective IRE1–XBP1 stress sensor results in the death of conventional dendritic cells in the lung, whereas those in the intestine survive due to a stronger ATF4-dependent stress response and RIDD activation.
Celià-Terrassa et al. find that by repressing LCOR, a modulator of the interferon response, miR-199a allows both normal and cancer mammary stem cells to evade senescence and differentiation, thus promoting tumorigenesis.
Bays et al. demonstrate that application of force to E-cadherin leads to LKB1-dependent activation of AMPK and recruitment of AMPK to E-cadherin complexes to increase glucose uptake and ATP production and re-enforce cell–cell junctions.
Lu et al. show that the choice between proteasomal degradation and selective autophagy is independent of the ubiquitin-binding properties of the receptors but largely determined by oligomerization potential.
