Catálogo de publicaciones - revistas

<jats:p>Controlling interfaces of phase-separating fluid mixtures is key to the creation of diverse functional soft materials. Traditionally, this is accomplished with surface-modifying chemical agents. Using experiment and theory, we studied how mechanical activity shapes soft interfaces that separate an active and a passive fluid. Chaotic flows in the active fluid give rise to giant interfacial fluctuations and noninertial propagating active waves. At high activities, stresses disrupt interface continuity and drive droplet generation, producing an emulsion-like active state composed of finite-sized droplets. When in contact with a solid boundary, active interfaces exhibit nonequilibrium wetting transitions, in which the fluid climbs the wall against gravity. These results demonstrate the promise of mechanically driven interfaces for creating a new class of soft active matter.</jats:p>

<jats:p>Hybridization between diverging lineages is associated with the generation and loss of species diversity, introgression, adaptation, and changes in reproductive mode, but it is unknown when and why it results in these divergent outcomes. We estimate a comprehensive evolutionary network for the largest group of unisexual vertebrates and use it to understand the evolutionary outcomes of hybridization. Our results show that rates of introgression between species decrease with time since divergence and suggest that species must attain a threshold of evolutionary divergence before hybridization results in transitions to unisexuality. Rates of hybridization also predict genome-wide patterns of genetic diversity in whiptail lizards. These results distinguish among models for hybridization that have not previously been tested and suggest that the evolutionary outcomes can be predictable.</jats:p>

<jats:p>Quantum information, communication, and sensing rely on the generation and control of quantum correlations in complementary degrees of freedom. Free electrons coupled to photonics promise novel hybrid quantum technologies, although single-particle correlations and entanglement have yet to be shown. In this work, we demonstrate the preparation of electron-photon pair states using the phase-matched interaction of free electrons with the evanescent vacuum field of a photonic chip–based optical microresonator. Spontaneous inelastic scattering produces intracavity photons coincident with energy-shifted electrons, which we employ for noise-suppressed optical mode imaging. This parametric pair-state preparation will underpin the future development of free-electron quantum optics, providing a route to quantum-enhanced imaging, electron-photon entanglement, and heralded single-electron and Fock-state photon sources.</jats:p>

<jats:p>Drug resistance in cancer is often linked to changes in tumor cell state or lineage, but the molecular mechanisms driving this plasticity remain unclear. Using murine organoid and genetically engineered mouse models, we investigated the causes of lineage plasticity in prostate cancer and its relationship to antiandrogen resistance. We found that plasticity initiates in an epithelial population defined by mixed luminal-basal phenotype and that it depends on elevated JAK and FGFR activity. Organoid cultures from patients with castration-resistant disease harboring mixed-lineage cells reproduce the dependency observed in mice, by upregulating luminal gene expression upon JAK and FGFR inhibitor treatment. Single-cell analysis confirms the presence of mixed lineage cells with elevated JAK/STAT and FGFR signaling in a subset of patients with metastatic disease, with implications for stratifying patients for clinical trials.</jats:p>

<jats:p>During gene transcription, RNA polymerase II (RNAPII) traverses nucleosomes in chromatin, but its mechanism has remained elusive. Using cryo-electron microscopy, we obtained structures of the RNAPII elongation complex (EC) passing through a nucleosome, in the presence of transcription elongation factors Spt6, Spn1, Elf1, Spt4/5, and Paf1C and the histone chaperone FACT. The structures show snapshots of EC progression on DNA, mediating downstream nucleosome disassembly followed by its reassembly upstream of the EC, facilitated by FACT. FACT dynamically adapts to successively occurring subnucleosome intermediates, forming an interface with the EC. Spt6, Spt4/5, and Paf1C form a “cradle” at the EC DNA-exit site, and support the upstream nucleosome reassembly. These structures explain the mechanism by which the EC traverses nucleosomes while maintaining the chromatin structure and epigenetic information.</jats:p>

<jats:p> Weiss <jats:italic>et al</jats:italic> . (Reports, 2 July 2021, p. 107) incorrectly conclude that the residence time for floating microplastic stock at the ocean surface is ~2.4 years. We contend that this conclusion is fundamentally flawed, because the residence time is obtained through dividing a published oceanic stock of plastic debris by a doubtable river microplastic flux estimated by the authors. </jats:p>

<jats:p> Many risk loci for Parkinson’s disease (PD) have been identified by genome-wide association studies (GWASs), but target genes and mechanisms remain largely unknown. We linked the GWAS-derived chromosome 7 locus (sentinel single-nucleotide polymorphism rs199347) to <jats:italic>GPNMB</jats:italic> through colocalization analyses of expression quantitative trait locus and PD risk signals, confirmed by allele-specific expression studies in the human brain. In cells, glycoprotein nonmetastatic melanoma protein B (GPNMB) coimmunoprecipitated and colocalized with α-synuclein (aSyn). In induced pluripotent stem cell–derived neurons, loss of <jats:italic>GPNMB</jats:italic> resulted in loss of ability to internalize aSyn fibrils and develop aSyn pathology. In 731 PD and 59 control biosamples, GPNMB was elevated in PD plasma, associating with disease severity. Thus, <jats:italic>GPNMB</jats:italic> represents a PD risk gene with potential for biomarker development and therapeutic targeting. </jats:p>

<jats:p> Mai <jats:italic>et al</jats:italic> . are mistaken in their assertions that we incorrectly calculated the residence time for floating microplastic stock at the ocean surface, and that most of our results are not novel. Their claim that our field-measured data and methods were not rigorous is wrong, as shown by a more careful consideration of what was done. </jats:p>

<jats:p> Predicting the function of noncoding variation is a major challenge in modern genetics. In this study, we used massively parallel reporter assays to screen 5706 variants identified from genome-wide association studies for both Alzheimer’s disease (AD) and progressive supranuclear palsy (PSP), identifying 320 functional regulatory variants (frVars) across 27 loci, including the complex 17q21.31 region. We identified and validated multiple risk loci using CRISPR interference or excision, including complement 4 ( <jats:italic>C4A</jats:italic> ) and <jats:italic>APOC1</jats:italic> in AD and <jats:italic>PLEKHM1</jats:italic> and <jats:italic>KANSL1</jats:italic> in PSP. Functional variants disrupt transcription factor binding sites converging on enhancers with cell type–specific activity in PSP and AD, implicating a neuronal SP1-driven regulatory network in PSP pathogenesis. These analyses suggest that noncoding genetic risk is driven by common genetic variants through their aggregate activity on specific transcriptional programs. </jats:p>