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Brd4, a reader of histone acetylation, is a transcriptional co-activator implicated in the maintenance of embryonic stem cells (ESCs). A study now shows that Brd4 is dispensable in mouse ESCs maintained in ground state pluripotency, and that cooperative activity of Tet1/2 and ESC-specific transcription factors compensates for its loss.
Mitochondria are critical for cellular energy generation and house oxidative phosphorylation (OXPHOS) complexes, which are under dual genetic control. A study finds that transcript translation and complex assembly are partitioned, and OXPHOS complexes III, IV and V are built at spatially defined regions of the mitochondrial inner membrane.
How the metabolic crosstalk between cancer and stromal cells affects tumour growth is incompletely defined. MYC-activated cancer cells are now shown to secrete exosomal miR-105, which fuels tumour growth by inducing a MYC-dependent metabolic programme in cancer-associated fibroblasts.
A coordinated DNA damage response mediated by p53 to repair DNA lesions or to promote apoptosis is essential for maintenance of genome stability. A study now unveils the long non-coding RNA GUARDIN as a component of this pathway, which protects genome integrity in a pleiotropic fashion.
The roles of transforming growth factor β (TGF-β) depend on the cellular context. Paraspeckle component 1 now arises as a driver of epithelial-to-mesenchymal transition and stemness transcription factors to redirect effectors from tumour suppressive to pro-metastatic gene promoters, emerging as a contextual determinant of TGF-β function.
During mouse back skin development, subsets of fibroblastic lineages transition from anti-fibrotic Engrailed-1 (En1) negative to pro-fibrotic En1-positive cells. Injuries of adult skin heal with scarring, whereas En1-deficient embryonic fibroblasts have the potential to promote scarless regeneration and repair.
The phosphatase PTEN is thought to govern tumour suppression predominantly through PI-3 kinase pathway regulation. A study now shows that a non-catalytic function of CK1α outcompetes the E3 ligase NEDD4-1 to stabilize PTEN, which activates FOXO3A-dependent ATG7 expression and stimulates tumour suppressive autophagy.
Regulation of pluripotency: Li and Belmonte review the pluripotency gene regulatory network, the molecular principles of pluripotency gene function, regulation by RNA-binding proteins and alternative splicing, heterogeneity and alternative pluripotency states.
N6-methyladenosine (m6A) mRNA modification influences mRNA fate by stimulating recruitment of m6A reader proteins. A previously unappreciated class of m6A reader proteins is now shown to use a common RNA-binding domain and flanking regions to selectively bind m6A-containing mRNAs, increasing their translation and stability.
Inflammation and reactive oxygen species (ROS) production after central nervous system injury are thought to enhance tissue damage and hamper neuronal regeneration. Evidence now suggests that NADPH2 oxidase delivery from macrophages to injured neurons through extracellular vesicles, promotes ROS signalling and axon recovery.
Exosomes are heterogeneous, nanoscale vesicles that mediate cellular communication. A study now leverages a size separation strategy to identify sub-classes of nanoparticles, revealing a subtype without an encapsulating membrane and variation in vesicle cargo, suggesting that size is not the only driver of heterogeneity.
Cytoplasmic flows are essential for various cellular processes. However, tools to manipulate these flows within cells are still lacking. Now research shows that an optical tool allows for control of cytoplasmic flows and can be used as a subcellular rheometer.
In this Review Article, Klionsky and co-authors discuss selective autophagy pathways that degrade unwanted cytosolic components and organelles, and how these pathways require ligand receptors and scaffold proteins for cargo specificity.
Autophagy and cancer: In this Review, Galluzzi and colleagues discuss the cellular and molecular mechanisms whereby autophagy functions in multiple aspects of malignant disease, including cancer initiation, progression and responses to therapy.
Mechanical forces influence both cytoplasmic and nuclear events. Kirby and Lammerding discuss recent evidence suggesting that the nucleus itself is a mechanosensor and methods to study nuclear mechanotransduction.
Mitochondria contain their own circular mitochondrial DNA (mtDNA), which, over time, is subjected to mutations that may eventually result in functional defects. A study now describes genetic and metabolic selection processes during germ cell development that prevent accumulation of harmful mtDNA variants.
Intrinsic factors that regulate dormancy of disseminated tumour cells (DTCs) are predominantly unknown. Now, knockdown of MSK1 is shown to accelerate bone metastasis of luminal breast cancer cells. MSK1 acts through epigenetic mechanisms that enforce the luminal phenotype and promote steady-state maintenance of DTCs within bone.
Elucidating regulation of mitochondrial mRNA translation will improve our understanding of mitochondrial function during homeostasis and disease. Ribonuclease EXD2 is now shown to be important for mitochondrial translation and oxidative phosphorylation, and its loss enhances ROS production, slows development and extends lifespan in flies.
Selective autophagy is important for controlled degradation of cellular components. However, a selective autophagic degradation mechanism for ribosomes in mammals has remained unclear. A study now describes non-selective and selective ribosome degradation and a significant role for ‘bystander’ non-selective autophagy.
