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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.
Liu, Zhang, Yao et al. report that IRE1 α clustering, known to be part of the unfolded protein response, is membrane-bound phase separation and that IRE1 can coalesce with the phase-separated stress granules.
Metastatic colonization involves cancer-cell-intrinsic mechanisms and microenvironmental interactions, and a better understanding of the factors that influence the final, post-extravasation phases is crucial for therapeutically targeting metatstasis.
Lindenhofer, Haendeler, Esk, Littleboy et al. perform whole-tissue lineage tracing in human cerebral organoids to reveal that a subpopulation of symmetrically dividing cells can adjust its lineage size depending on tissue demands.
Yang, Golkaram et al. reported that in human embryonic stem cells, cellular crowding leads to the blockade of FGFR1 endocytosis, resulting in a decrease in ETV4 expression. This, in turn, derepresses the neuroectoderm fate.
Xin et al. show, through intravital imaging, that KrasG12D induces epithelial tissue deformation in a spatiotemporally specific manner by converting the pulsatile ERK signal fluctuation in stem cells into sustained activation.
We show that the mitochondrial fission proteins MiD49 and MiD51 are activated by fatty acyl-coenzyme A (FA-CoA). FA-CoA binds in a previously identified pocket located within MiDs, inducing their oligomerization and ability to activate the dynamin DRP1, ultimately promoting mitochondrial fission. Activated MiDs synergize with mitochondrial fission factor (MFF) in stimulating DRP1 activity, leading us to hypothesize that MiDs act upstream of MFF during mitochondrial fission.
Our understanding of the basic mechanisms of autophagy is growing, but many questions remain about the types of autophagy cells use, when they use them, and how they function in different contexts. We asked emerging and established leaders in the field to discuss the questions and areas that they are most excited about to deepen our understanding of autophagy.
Reicher, Reiniš et al. report a method for multicolour tagging using genome-scale intron-targeting sgRNA libraries that, in combination with computer vision, enables the systematic detection of protein localization changes.
Volume electron microscopy (vEM) generates large 3D volumes of cells or tissues at nanoscale resolutions, enabling analyses of organelles in their cellular environment. Here, we provide examples of vEM in cell biology and discuss community efforts to develop standards in sample preparation and image acquisition for enhanced reproducibility and data reuse.