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ESCRT-III seals holes in the nuclear envelope (NE). A study now shows that the Cmp7-directed ESCRT-III cascade that grommets and reseals NE holes after spindle pole body (SPB) extrusion at the end of fission yeast mitosis is complemented by the presence of a proteinaceous diffusion barrier to ensure NE integrity.
In many species, maternally deposited Piwi-interacting RNAs (piRNAs) deliver intergenerational epigenetic information to protect progeny from transposon expansion or invasion. However, Y-chromosome-encoded piRNAs cannot be passed from mothers to male offspring, yet mothers use autosomally encoded piRNAs to allow sons to utilize their Y chromosome to protect against ‘selfish’ elements.
The molecular program of human germline commitment remains largely unknown. A new study delineates the multifaceted functions of DMRT1 in human germline development, particularly in the transition from early to late primordial germ cells.
RNA modifications have emerged as key gene regulators. A new study shows that increased levels of reactive oxygen species in cancer induce widespread, sequence-specific modifications of guanines in the seed regions of microRNAs, altering the targets of those miRNAs and influencing tumorigenesis.
Embryonic diapause in development and paused pluripotency in embryonic stem cells result in a state of hypotranscription through mechanisms that remain unclear. A new study dissects the role of METTL3-deposited global m6A RNA methylation in mediating this transcriptional dormancy.
Genetic clearance of p16high senescent cells or the use of senolytics improved the efficacy of stem cell reprogramming in vitro and in vivo, and helped establish induced pluripotent stem cells with features of experimental totipotency. When ablation of p16high senescent cells was combined with partial four-factor reprogramming in vivo, we observed noticeable histopathological liver rejuvenation in aged mice.
Pathways linked to the modification of RNA with N6-methyladenosine (m6A) are known to be involved in initiating and maintaining cancer. But many of the key components of these pathways remain undiscovered. The RBFOX2 protein has now been identified as an m6A reader involved in locus-specific chromatin regulation, with therapeutic implications for myeloid leukaemia.
The interaction of non-immune and immune cells in the tumour microenvironment (TME) determines the quality of the immune attack on nascent tumour cells. A new study in melanoma cells shows that specific histone variants dampen the expression of cytokine genes in cancer-associated fibroblasts, leading to an immunosuppressive TME.
The mechanisms controlling lysosome abundance in cells and how changes in lysosome pool size impact physiological and pathophysiological processes are discussed.
Cells use various metabolic pathways to synthesize the building blocks for growth and proliferation. To ensure balanced growth, these biosynthetic processes must be tightly coordinated. We describe a molecular machinery that senses the cellular capacity to make lipids to regulate other biosynthetic processes — such as protein synthesis — accordingly.
A fast protocol for chemical cellular reprogramming reveals a diapause-like state, endogenous retrovirus activation and barriers to cell-fate transitions on the way to pluripotency. The system offers insights into manipulation of cellular regeneration and rejuvenation, two processes with great therapeutic potential.
In many species, a mother’s environment can impact offspring’s metabolism, but the mechanisms that mediate such intergenerational effects are unclear. In this issue, a study finds that the provisioning of a sphingolipid from mothers to offspring drives changes in offspring metabolism that protect against neuronal damage.
Sphingomyelin synthase 2 foci assemble at the leading edge of the basal membrane in migrating cells, and these foci eventually become sites of migrasome formation. Conversion of ceramide to sphingomyelin spurs migrasome growth and preserves the structural integrity of these organelles.
Pioneer transcription factors bind closed chromatin regions, alter local accessibility and activate target genes. A study reveals that the SOX9 transcription factor drives cell fate switching by activating hair follicle cell enhancers, while simultaneously repressing epidermal enhancers via sequestration of epigenetic factors.
Molecular insight into mechanisms that mediate the selective autophagy of lipid droplets (that is, lipophagy) has been lacking. This study identifies spartin, a protein mutated in a complex hereditary spastic paraplegia called Troyer syndrome, as a receptor that targets lipid droplets to the lysosome for degradation.
The Human BioMolecular Atlas Program (HuBMAP) presents its production phase: the generation of spatial maps of functional tissue units across organs from diverse populations and the creation of tools and infrastructure to advance biomedical research.
Reprogramming of somatic cells is an inherently inefficient process. A new study has now identified histone H3K36 methylation as a crucial reprogramming barrier that operates downstream of TGFβ signalling. Global inhibition of H3K36 methylation induced PRC2-dependent silencing of mesenchymal genes and dramatically increased reprogramming efficiency.
Class 3 phosphatidylinositol-3-kinase (PI3K) has a surprising nuclear function as a coactivator of the circadian clock Bmal1–Clock transcription factor complex for rhythmic purine nucleotide metabolism. This finding opens new avenues for establishing the roles of nuclear subunits of class 3 PI3K in metabolic homeostasis.
The compact state of chromatin induced by the methylation of lysine 9 on histone H3 has long been implicated in a heritable state of transcriptional repression. A study now shows that transient deposition of H3K9me3 helps to stabilize stalled DNA replication forks, while its reversal enables accurate fork restart.
The PHD–pVHL pathway is essential for oxygen-dependent prolyl hydroxylation of HIFA. A recent study identifies RIPK1 as a hydroxylation target in this pathway during hypoxia-induced cell death and presents a 2.8 Å resolution crystal structure of the pVHL–elongin B/C complex bound to hydroxylated RIPK1.
