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Kathiriya et al. report that fibrotic signalling in the lung mesenchyme leads to transdifferentiation of human alveolar type 2 cells into KRT5+ basal cells, providing a mechanistic explanation for the pathology associated with severe lung injuries.
Guo et al. show that H3.3 prevents the premature exhaustion of HSCs and differentiation into granulocyte-macrophage progenitors by safeguarding the interplay between H3K27me3 and H3K9me3 marks.
Zhang et al. identify and characterize supermeres as extracellular nanoparticles that exhibit unique biological and functional properties with potential prognostic and therapeutic value across distinct diseases.
Gerber, Russ et al. show that the H3.3 chaperone Daxx, which represses endogenous retroviral and retrotransposable elements, acts as an epigenetic barrier to control haematopoietic progenitor plasticity and protect against PU.1-mediated inflammation.
Juste, Kaushik and co-workers show that the circadian regulation of chaperone-mediated autophagy orchestrates the degradation of clock components and contributes to the circadian remodelling of the proteome.
Wang et al. analysed post-mortem samples of the lungs of patients with COVID-19 by bulk and single-nucleus RNA sequencing along with proteomics and discovered lung senescence as a feature of COVID-19 pathology.
Jo et al. develop a broadly applicable deep-learning approach to predict fluorescence (FL) based on label-free refractive index (RI) measurements, ‘RI2FL’ (RI to FL). The trained model can be used across cell types without retraining.
By characterizing the composition of mitochondrial-derived vesicles (MDVs), König et al. define a MIRO1/2- and DRP1-dependent MDV biogenesis pathway and propose that MDVs maintain the mitochondrial proteome by shuttling assembled protein complexes to lysosomes.
Fatehullah et al. develop transgenic and orthotopic mouse models to recapitulate advanced human gastric cancer and uncover a mechanistic role for Lgr5+ stem-like cells in promoting disease initiation and progression.
Adamowicz et al. report that toxic PARP1 activity, induced by ataxia-associated mutations in XRCC1, impairs the recovery of global transcription during DNA base excision repair by promoting aberrant recruitment and activity of the histone ubiquitin protease USP3.
Hogan and colleagues report that the RNA helicase Ddx21 mediates Vegfc-stimulated lymphangiogenesis during zebrafish development through controlling rDNA transcription and ribosome biogenesis in endothelial cells.
Piazza et al. report that following double-strand break (DSB) formation in S. cerevisiae, cohesin at DSBs facilitates local homology search during repair by homologous recombination, while suppressing DSB contacts with genome-wide double-strand DNAs.
Li et al. define an adaptive resistance mechanism against FGFR inhibitor treatment in breast cancer attributed to loss of BRG1 chromatin recruitment, reactivation of YAP-dependent enhancers and upregulation of amino acid-induced mTORC1 activity.
Mehidi et al. show that piconewton forces exerted by the polymerization of individual actin filaments displace the WAVE regulatory complex from lamellipodial tips, thereby regulating WAVE complex activity during cell migration.
Gasser and colleagues report that H3K9me2 and H3K9me3 repress lineage-specific and germline genes by restricting the activity of a subset of transcription factors in terminally differentiated Caenorhabditiselegans tissues.
Frede et al. perform single-cell transcriptome and chromatin accessibility profiling of immune cells isolated from patients with refractory multiple myeloma before or during the course of chemotherapy.
Cereghetti et al. report that the glycolytic metabolite fructose-1,6-bisphosphate initiates the disassembly of amyloids formed by the yeast pyruvate kinase Cdc19 to resume ATP production during stress recovery.
Löbrich and colleagues report that RAD52 and BRCA2 limit polymerase θ activity until the onset of mitosis to ensure double-strand breaks arising in the S phase are repaired by polymerase θ-mediated end joining in mitosis, not in S phase.
Lu et al. demonstrate that allergens induce the formation of eosinophil extracellular traps, which activate pulmonary neuroendocrine cells to secrete neuropeptides and neurotransmitters as well as amplify allergic immune responses.
Moreno-Layseca et al. identify Swip1 as an integrin-specific endocytic adaptor controlling the dynamics of integrin adhesion complexes as well as the migration and invasion of breast cancer cells.