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Chromosome-scale and haplotype-resolved assembly of Pinus densiflora sheds light on Pinus-specific genome enlargement. Comparison between haplotypes and resequencing of 30 wild accessions show allelic imbalance with roles in flowering regulation and stress resistance.

Damaged lysosomes are eliminated by lysophagy, yet the regulatory mechanisms of this process are not fully defined. Here, the authors identify that the TBK1-SCFFBXO3-TMEM192-TAX1BP1 axis is essential for lysosome degradation, with FBXO3 functioning in lysosome integrity.

The quark structure of the f₀(980) hadron is still unknown after 50 years of its discovery. Here, the CMS Collaboration reports a measurement of the elliptic flow of the f₀(980) state in proton-lead collisions at a nucleon-nucleon centre-of-mass energy of 8.16 TeV, providing strong evidence that the state is an ordinary meson.

p62/SQSTM1 acts as a key mediator in the selective autophagy of protein aggregates, or aggrephagy. Here the authors identify the prefoldin-like chaperone UXT as an autophagy adaptor of p62 dependent aggrephagy and show that ectopic UXT expression delays motor neuron degeneration in a Xenopus model.

Islet amyloid polypeptide (IAPP) deposition is associated with islet cell loss in diabetes. Here the authors show that a small molecule autophagy enhancer reduces IAPP accumulation in vitro, and also improves glucose tolerance in hIAPP⁺ mice fed high-fat diet, accompanied by reduced hIAPP accumulation, in vivo.

Polygenic scores for body mass index and obesity constructed using data from 5 million people with different ancestries were associated with distinct weight gain trajectories from early childhood to adulthood.

L1 is a group of active retrotransposons in humans. Here the authors show that m⁶A modifications on L1 RNA increase translation efficiency and retrotransposition in human cells. M⁶A motifs are more enriched in evolutionary young L1s.

Brown adipose tissue (BAT) is a specialized thermogenic organ that undergoes high demands of protein synthesis during thermogenic adaptation. Here, the authors show that the cold responsive phosphatase Ssu72 is required for mRNA translation that affects thermogenic adaptation in BAT.

Vascular calcification (VC) increases morbidity and mortality in cardiovascular and metabolic diseases. Here, Kwon et al.show that calcification stimuli induce MDM2- mediated ubiquitination and proteasomal degradation of HDAC1, suggesting a possible therapeutic strategy for treatment of VC patients.

Ageing leads to a loss of muscle mass and strength, called sarcopenia. Here, the authors show that fatty acid binding protein 3 (FABP3), a lipid chaperone, drives age-dependent lipidome remodeling in skeletal muscle and deteriorates muscle mass and contractility by modulating membrane fluidity and ER stress signaling.

The Ssu72 phosphatase is required to prevent premature separation of sister chromatids during interphase. Kim et al.show that this signal is terminated at early mitosis by Aurora B, which phosphorylates Ssu72 and promotes its ubiquitin-dependent degradation.

Wang et al. show how glucose sensing via O-GlcNAcylation drives the assembly of a glycolytic metabolon on the mitochondrial surface to couple metabolic efficiency with neuronal activity.

Rapid detection of antiviral resistant strains is important for effective clinical treatment. Here the authors develop an antibody which specifically binds to multidrug-resistant influenza virus and demonstrated detection in a number of different systems using the antibody.

Angiogenesis is a complex process that requires coordinated changes in endothelial cell behavior. Here the authors use Ribo-tag and RNA-Seq to determine temporal profiles of transcriptional activity during postnatal retinal angiogenesis, identifying transcriptional regulators of the process.

Accurate segmentation of ischemic stroke lesions from brain MRI is crucial for timely diagnosis and treatment planning. Here, the authors present DeepISLES, an AI ensemble for stroke MRI analysis that outperforms previous methods and matches expert radiologist performance in identifying stroke lesions.

Analyses of 2,658 whole genomes across 38 types of cancer identify the contribution of non-coding point mutations and structural variants to driving cancer.

Ca2+ overload-induced mitochondrial dysfunction is considered a contributing factor alcohol-associated liver disease pathogenesis. Here the authors report that PDK4 promotes Ca2 + -channelling complex formation at the endoplasmic reticulum-mitochondria contact sites, which contributes to the pathogenesis of alcohol-associated liver disease in studies with male mouse and hepatocyte models.

A gold-embedded oxide interlayer can be used to create metal–interlayer–semiconductor contacts for two-dimensional materials that exhibit low series resistance and Fermi level depinning.

Virtual memory T cells have antimicrobial functions but whether they can contribute to inflammatory pathology is unclear. Here the authors show that a subset of CD8⁺ T cells that originates from virtual memory T cells upon cytokine stimulation can drive the chronic inflammatory disease alopecia areata via innate-like cytotoxic effector functions.

The initiation of translation is a highly regulated process that contributes to specific gene expression programs. Here the authors find that, in vertebrate, threonyl-tRNA synthetase (TRS) can act as a scaffold for the initiation machinery to stimulate the translation of a specific set of mRNAs.

The mechanisms underlying diabetic neuropathy remain elusive. Here, the authors identify that UCHL1 deubiquitinase positively regulates insulin signaling and its loss leads to axonal degeneration of sensory neurons.

RNA G-quadruplex is a secondary RNA structure formed by G-rich sequences. Now a zinc-finger protein has been identified to target the G-quadruplex motifs of two key factors in phloem differentiation, leading to a new translational regulatory pathway.

Nonsense-mediated mRNA decay (NMD) is a translation-coupled process that eliminates mRNAs containing premature translation-termination codons. Here the authors identify a role for the NMD factor UPF1 in protein quality control, whereby truncated misfolded polypeptides are cleared through autophagy.

Cas9 and Cpf1 have both been adapted for genome engineering, editing and gene expression regulation. Here the authors design a fusion guide RNA that can interact with both proteins for multiple and orthogonal genome manipulation.

Leucyl-tRNA synthetase (LRS) is a leucine sensor of the mTORC1 pathway. Here, the authors identify inhibitors of the GTPase activating function of LRS, not affecting its catalytic activity, and demonstrate that the leucine sensor function of LRS can be a new target for mTORC1 inhibition.

This study shows that plants form epidermal cells anew to protect a vulnerable new surface exposed by organ abscission while facilitating the subsequent growth of tissue and fruit at the abscission site.

Federated learning (FL) algorithms have emerged as a promising solution to train models for healthcare imaging across institutions while preserving privacy. Here, the authors describe the Federated Tumor Segmentation (FeTS) challenge for the decentralised benchmarking of FL algorithms and evaluation of Healthcare AI algorithm generalizability in real-world cancer imaging datasets.

Here, the authors show that higher levels of the gut bacterial clade TANB77 associate with better response to cancer immunotherapy, and further demonstrate in mice that a conserved pilin from TANB77 plays a role in enhancing immunotherapy efficacy, suggesting a potential therapeutic avenue.

Leucyl-tRNA synthetase 1 (LARS1) is a leucine sensor for mTORC1 signaling and regulates leucine utilization depending on glucose availability. Here, the author show that O-GlcNAcylation of LARS1 is crucial for its ability to regulate mTORC1 activity and leucine metabolism upon glucose starvation.

The genetic link between placenta function and congenital heart defects has been established, though the cellular mechanisms underlying this connection is less clear. Here they show that PIBF1 regulates syncytiotrophoblast fusion and that loss of PIBF1 also negatively impacts heart development, providing a potential link between the development of these two organs.