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Unconventional quasiparticles emerging in the fractional quantum Hall regime 1,2 present the challenge of observing their exotic properties unambiguously. Although the fractional charge of quasiparticles has been demonstrated for nearly three decades 3-5 , the first convincing evidence of their anyonic quantum statistics has only recently been obtained 6,7 and, so far, the so-called scaling dimension that determines the propagation dynamics of the quasiparticles remains elusive. In particular, although the nonlinearity of the tunnelling quasiparticle current should reveal their scaling dimension, the measurements fail to match theory, arguably because this observable is not robust to non-universal complications 8-12 . Here we expose the scaling dimension from the thermal noise to shot noise crossover and observe an agreement with expectations. Measurements are fitted to the predicted finite-temperature expression involving both the scaling dimension of the quasiparticles and their charge 12,13 , in contrast to previous charge investigations focusing on the high-bias shot-noise regime 14 . A systematic analysis, repeated on several constrictions and experimental conditions, consistently matches the theoretical scaling dimensions for the fractional quasiparticles emerging at filling factors ν = 1/3, 2/5 and 2/3. This establishes a central property of fractional quantum Hall anyons and demonstrates a powerful and complementary window into exotic quasiparticles., (© 2024. The Author(s).)

In 1909, Millikan showed that the charge of electrically isolated systems is quantized in units of the elementary electron charge e. Today, the persistence of charge quantization in small, weakly connected conductors allows for circuits in which single electrons are manipulated, with applications in, for example, metrology, detectors and thermometry. However, as the connection strength is increased, the discreteness of charge is progressively reduced by quantum fluctuations. Here we report the full quantum control and characterization of charge quantization. By using semiconductor-based tunable elemental conduction channels to connect a micrometre-scale metallic island to a circuit, we explore the complete evolution of charge quantization while scanning the entire range of connection strengths, from a very weak (tunnel) to a perfect (ballistic) contact. We observe, when approaching the ballistic limit, that charge quantization is destroyed by quantum fluctuations, and scales as the square root of the residual probability for an electron to be reflected across the quantum channel; this scaling also applies beyond the different regimes of connection strength currently accessible to theory. At increased temperatures, the thermal fluctuations result in an exponential suppression of charge quantization and in a universal square-root scaling, valid for all connection strengths, in agreement with expectations. Besides being pertinent for the improvement of single-electron circuits and their applications, and for the metal-semiconductor hybrids relevant to topological quantum computing, knowledge of the quantum laws of electricity will be essential for the quantum engineering of future nanoelectronic devices.

Many-body correlations and macroscopic quantum behaviours are fascinating condensed matter problems. A powerful test-bed for the many-body concepts and methods is the Kondo effect, which entails the coupling of a quantum impurity to a continuum of states. It is central in highly correlated systems and can be explored with tunable nanostructures. Although Kondo physics is usually associated with the hybridization of itinerant electrons with microscopic magnetic moments, theory predicts that it can arise whenever degenerate quantum states are coupled to a continuum. Here we demonstrate the previously elusive 'charge' Kondo effect in a hybrid metal-semiconductor implementation of a single-electron transistor, with a quantum pseudospin of 1/2 constituted by two degenerate macroscopic charge states of a metallic island. In contrast to other Kondo nanostructures, each conduction channel connecting the island to an electrode constitutes a distinct and fully tunable Kondo channel, thereby providing unprecedented access to the two-channel Kondo effect and a clear path to multi-channel Kondo physics. Using a weakly coupled probe, we find the renormalization flow, as temperature is reduced, of two Kondo channels competing to screen the charge pseudospin. This provides a direct view of how the predicted quantum phase transition develops across the symmetric quantum critical point. Detuning the pseudospin away from degeneracy, we demonstrate, on a fully characterized device, quantitative agreement with the predictions for the finite-temperature crossover from quantum criticality.

Cell migration requires the generation of branched actin networks that power the protrusion of the plasma membrane in lamellipodia. The actin-related proteins 2 and 3 (Arp2/3) complex is the molecular machine that nucleates these branched actin networks. This machine is activated at the leading edge of migrating cells by Wiskott-Aldrich syndrome protein (WASP)-family verprolin-homologous protein (WAVE, also known as SCAR). The WAVE complex is itself directly activated by the small GTPase Rac, which induces lamellipodia. However, how cells regulate the directionality of migration is poorly understood. Here we identify a new protein, Arpin, that inhibits the Arp2/3 complex in vitro, and show that Rac signalling recruits and activates Arpin at the lamellipodial tip, like WAVE. Consistently, after depletion of the inhibitory Arpin, lamellipodia protrude faster and cells migrate faster. A major role of this inhibitory circuit, however, is to control directional persistence of migration. Indeed, Arpin depletion in both mammalian cells and Dictyostelium discoideum amoeba resulted in straighter trajectories, whereas Arpin microinjection in fish keratocytes, one of the most persistent systems of cell migration, induced these cells to turn. The coexistence of the Rac-Arpin-Arp2/3 inhibitory circuit with the Rac-WAVE-Arp2/3 activatory circuit can account for this conserved role of Arpin in steering cell migration.

Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.

Here we report a high-quality draft genome sequence of the domestic dog (Canis familiaris), together with a dense map of single nucleotide polymorphisms (SNPs) across breeds. The dog is of particular interest because it provides important evolutionary information and because existing breeds show great phenotypic diversity for morphological, physiological and behavioural traits. We use sequence comparison with the primate and rodent lineages to shed light on the structure and evolution of genomes and genes. Notably, the majority of the most highly conserved non-coding sequences in mammalian genomes are clustered near a small subset of genes with important roles in development. Analysis of SNPs reveals long-range haplotypes across the entire dog genome, and defines the nature of genetic diversity within and across breeds. The current SNP map now makes it possible for genome-wide association studies to identify genes responsible for diseases and traits, with important consequences for human and companion animal health.