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Ma, Cao et al. uncover dynamic changes of chromatin reorganization in progenitor B cells during ageing, associated with altered H3K27ac levels and expression of genes that are critical for B cell development.
With a shRNA targeted screen, Ferrer, Cho, Boon et al. identify a role for Gstt1 in enhancing epithelial–mesenchymal transition and disseminated tumour cell features in a subset of slow-cycling cells, thereby facilitating metastatic progression.
Ferroptosis is a form of cell death that is characterized by morphological abnormalities of mitochondria and the overwhelming peroxidation of phospholipids. Certain tumours are susceptible to ferroptosis, which could be exploited to treat cancers.
Wu, Zhao, Shin and Yin show that the RNA–RNA-binding protein complex LOC–DHX15 drives microglia infiltration into the tumour microenvironment in glioblastoma and suggest targeting this complex as a potential treatment strategy.
Aminoacyl-tRNA synthetases can promote or suppress cancer progression by regulating codon-dependent translation. A study now shows that valine aminoacyl-tRNA synthetase (VARS) promotes therapeutic resistance of melanoma to MAPK pathway inhibitors by enhancing translation of valine-enriched genes, including the fatty acid oxidation gene HADH.
El-Hachem et al. show that MAPK therapy upregulates valine aminoacyl-tRNA synthetase and alters fatty acid oxidation by promoting translation of valine-enriched transcripts, providing a resistance mechanism that may be therapeutically targeted.
Batki, Hetzel et al. report a lineage-tracing strategy to track extraembryonic gut endoderm cells over development. They find that these cells are eventually eliminated in a p53-dependent manner and neighbouring embryonic cells clear their remnants.
Oocyte development involves the prolonged and intricate process of building a distinctive transcriptome and epigenome to anticipate embryogenesis after fertilization. Research now shows that mouse oocytes use an unusual chromatin signature to mark regulatory elements, and that the transcription factors TCF3 and TCF12 have a key role.
Liu, Xie and colleagues profile putative cis-regulatory elements in mouse oocytes and pre-implantation embryos. They further validate putative enhancers in oocytes and identify the transcription factors TCF3 and TCF12 as key regulators of folliculogenesis.
Jungnickel, Guelle et al. use metabolomics, electrophysiology and cryo-EM approaches to show that MFSD1 is a lysosomal dipeptide uniporter, which provides an additional route to recycle lysosomal proteolysis products to lysosomal amino acid exporters.
Sensing stress within the endoplasmic reticulum (ER), the ER transmembrane protein IRE1α initiates a signal transduction pathway to restore homeostasis. A study finds that this process requires an ER membrane-bound phase separation event that leads to the local assembly of stress granules (SGs) and delivery of signalling components.
Mitochondrial damage in stress conditions results in the release of mitochondrial DNA (mtDNA), causing inflammation that is linked to various diseases. We discovered a mechanism for the elimination of this harmful mtDNA — ‘nucleoid-phagy’. Targeting this process represents another way to treat mitochondrial damage-related diseases.
Machitani, Nomura and colleagues report that hTERT suppresses R-loops through its RNA-dependent RNA polymerase activity and protects against genome instability.
Biological clocks can be used to evaluate the age of a cell or organisms. This Perspective proposes the concept of an intrinsically disordered protein (IDP) clock, whereby the aggregation state of an IDP encodes for a biological ageing signature.
Liu, Zhen, Xie, Luo, Zeng, Zhao et al. show that the major nucleoid protein TFAM interacts with cytoplasmic LC3B during oxidative or inflammatory stress to attenuate mitochondrial DNA-induced inflammation via the cGAS–STING pathway.
Granath-Panelo and Kajimura review emerging evidence of mitochondrial heterogeneity in different contexts and discuss how mitochondrial malleability contributes to cell fate determination and tissue remodelling.
Yang et al. report that the nucleolar protein fibrillarin (FBL) affects acute myeloid leukaemia (AML) cell function through biomolecular condensation-dependent regulation of early pre-rRNA processing and translation.
Aviner et al. show that translation and aggregation of Huntingtin (HTT) are regulated by a stress-responsive upstream open reading frame. Mutant HTT depletes translation elongation factor eIF5A, leading to ribosome pausing and collisions.
Two new landmark studies use innovative and complementary lineage tracing approaches in human cerebral organoids to reveal symmetric stem cell division and direct neurogenesis of basal radial glial cells to enable cortical growth, expansion and differentiation.