Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
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.
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.