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Different gut microbial metabolites have the potential to promote and protect against colorectal cancer (CRC). A study now links trans-3-indoleacrylic acid (IDA), a metabolite derived from Peptostreptococcus anaerobius, with colorectal carcinogenesis through a distinct ferroptosis pathway AHR–ALDH1A3–FSP1–CoQ10.
The structures and functions of organelles are highly interdependent. Using paired 3D electron microscopy and multi-omics, a study now shows how other organelles affect mitochondrial structure and function: peroxisome-derived lipids reverse mitochondrial stress, highlighting the importance of organelle interconnectivity.
Lineage plasticity and epigenetic changes underlie prostate development and cancer evolution. A new study shows that basal and luminal prostate cells have distinct metabolic profiles, with a basal-to-luminal shift intensifying pyruvate oxidation. Metabolic changes in turn influence chromatin architecture, lineage reprogramming and treatment sensitivity.
There is increasing interest in approaches that target and eliminate senescent cells. A study reports that the coatomer complex I (COPI) pathway is important for the survival of senescent cells, and suggests that targeting this pathway could hold therapeutic promise in the context of senescence-associated diseases.
The main barriers for intracellular receptors to sense circulating pathogen-associated molecular patterns (PAMPs) is how these PAMPs enter the cells. A study reveals that extracellular vesicles (EVs) bind lipopolysaccharide (LPS) via the lipid bilayer and mediates LPS intracellular transfer in a CD14-dependent endocytosis to activate noncanonical NLRP3 inflammasome and pyroptosis.
Cells use diverse mechanisms to rid themselves of dysfunctional or excess mitochondria. A study now shows that C. elegans sperm use a previously undescribed mechanism to rapidly expel single healthy mitochondria in membrane-bound structures called mitophers.
YTHDF family members are ‘readers’ of a common mRNA modification, but their effects on mRNA translation and stability have been disputed. A new study shows that YTHDF1 and YTHDF3 are post-translationally regulated through O-GlcNAcylation, unifying disparate results and pointing to environmental cues that could modulate YTHDF function.
How spatial organization in the cell is achieved on the organelle scale is unclear. A new study finds that tethering specific proteins near the surface of micelle-like paraspeckles modifies their properties and determines whether these subnuclear organelles are separate from, adhere to, or are engulfed by nuclear speckles.
The bacterial pathogen Legionella pneumophila uses effectors — toxins — to facilitate pathogenesis within host cells. A recent study identifies dual mechanisms of the effector SidI as an inhibitor of translation elongation. The N-terminal domain mimics tRNA, whereas the C-terminal domain glycosylates the ribosome.
Disruption of ribosome assembly results in the accumulation of aggregation-prone ‘orphaned’ ribosomal proteins that are toxic to cells if left unchecked. A study finds that cells store such ribosomal proteins during heat shock to enable a quick recovery of ribosome assembly after the removal of this stress.
Bone marrow endothelial cells deliver oxygen and nutrients and regulate bone formation and haematopoiesis in the surrounding microenvironment. A new study identifies a subtype of capillary that occurs exclusively in the epiphysis and displays unique characteristics that have a role in balancing osteogenesis and haematopoiesis.
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.
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.
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.
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.
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.