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Among the wealth of single fluorescent defects recently detected in silicon, the G center catches interest for its telecom single-photon emission that could be coupled to a metastable electron spin triplet. The G center is a unique defect where the standard Born-Oppenheimer approximation used in solid-state physics breaks down as one of its atoms, a silicon atom in interstitial position Si_{(i)}, can move between six sites. The impact of its displacement, due either to coherent tunneling or to random jumps from one site to another, on the optical properties of G centers is still largely unknown, especially in silicon-on-insulator (SOI) samples. Here, we investigate the displacement of the center of mass of the G center in silicon. By performing photoluminescence experiments at single-defect scale, we show that individual G defects in SOI exhibit several emission dipoles and zero-phonon line fine structures with splittings up to approximately 1 meV, both indicating a motion of the defect central atom over time. Combining polarization and spectral analysis at the single-photon level, we evidence that the reconfiguration dynamics is drastically different from the one of the unperturbed G center in bulk silicon where the mobile atom is fully delocalized over all six sites through tunneling. The SOI structure freezes the Si_{(i)} delocalization of the G defect and, as a result, enables one to isolate linearly polarized optical lines. Under above-band-gap optical excitation, the central atom of G centers in SOI behaves as if it were in a six-slot roulette wheel, randomly alternating between localized crystal sites at each optical cycle. Comparative measurements in a bulk silicon sample and ab initio calculations highlight that strain is likely the dominant perturbation impacting the G center geometry. These results shed light on the importance of the atomic reconfiguration dynamics to understand and control the photoluminescence properties of the G center in silicon. More generally, these findings emphasize the impact of strain fluctuations inherent to SOI wafers for future quantum integrated photonics applications based on color centers in silicon.

In this manuscript, Finco et al demonstrate the use of a quantum magnetometer based on a single NV centre for all-optical imaging of antiferromagnetic (AFM) spin textures. By exploiting variations of the NV spin relaxation rate, they succeed in imaging AFM domain walls and skyrmions.

Designing efficient nonlinear dynamic resonances for weak signal amplification remains a challenge. Here, the authors demonstrate a resonance manipulation strategy able to enhance weak signals in a nonlinear oscillator consisting of an optically-probed driven nano-electromechanical resonator.

Systemic lupus erythematosus (SLE) is a severe and heterogeneous autoimmune disease with a complex genetic etiology, characterized by the production of various pathogenic autoantibodies, which participate in end-organ damages. The majority of human SLE occurs in adults as a polygenic disease, and clinical flares interspersed with silent phases of various lengths characterize the usual evolution of the disease in time. Trying to understand the mechanism of the different phenotypic traits of the disease, and considering the central role of B cells in SLE, we previously performed a detailed wide analysis of gene expression variation in B cells from quiescent SLE patients. This analysis pointed out an overexpression of TRIB1. TRIB1 is a pseudokinase that has been implicated in the development of leukemia and also metabolic disorders. It is hypothesized that Trib1 plays an adapter or scaffold function in signaling pathways, notably in MAPK pathways. Therefore, we planned to understand the functional significance of TRIB1 overexpression in B cells in SLE. We produced a new knock-in model with B-cell-specific overexpression of Trib1. We showed that overexpression of Trib1 specifically in B cells does not impact B cell development nor induce any development of SLE symptoms in the mice. By contrast, Trib1 has a negative regulatory function on the production of immunoglobulins, notably IgG1, but also on the production of autoantibodies in an induced model. We observed a decrease of Erk activation in BCR-stimulated Trib1 overexpressing B cells. Finally, we searched for Trib1 partners in B cells by proteomic analysis in order to explore the regulatory function of Trib1 in B cells. Interestingly, we find an interaction between Trib1 and CD72, a negative regulator of B cells whose deficiency in mice leads to the development of autoimmunity. In conclusion, the overexpression of Trib1 could be one of the molecular pathways implicated in the negative regulation of B cells during SLE.

To generate highly specific and adapted immune responses, B cells diversify their antibody repertoire through mechanisms involving the generation of programmed DNA damage. Somatic hypermutation (SHM) and class switch recombination (CSR) are initiated by the recruitment of activation-induced cytidine deaminase (AID) to immunoglobulin loci and by the subsequent generation of DNA lesions, which are differentially processed to mutations during SHM or to double-stranded DNA break intermediates during CSR. The latter activate the DNA damage response and mobilize multiple DNA repair factors, including Parp1 and Parp2, to promote DNA repair and long-range recombination. We examined the contribution of Parp3 in CSR and SHM. We find that deficiency in Parp3 results in enhanced CSR, while SHM remains unaffected. Mechanistically, this is due to increased occupancy of AID at the donor (Sμ) switch region. We also find evidence of increased levels of DNA damage at switch region junctions and a bias towards alternative end joining in the absence of Parp3. We propose that Parp3 plays a CSR-specific role by controlling AID levels at switch regions during CSR.

Cavity optomechanical systems with an enhanced coupling between mechanical motion and electromagnetic radiation have permitted the investigation of many novel physical effects. The optomechanical coupling in the majority of these systems is of dispersive nature: the cavity resonance frequency is modulated by the vibrations of the mechanical oscillator. Dissipative optomechanical interaction, where the photon lifetime in the cavity is modulated by the mechanical motion, has recently attracted considerable interest and opens new avenues in optomechanical control and sensing. In this work we demonstrate an external optical control over the dissipative optomechanical coupling strength mediated by the modulation of the absorption of a quantum dot layer in a hybrid optomechanical system. Such control enhances the capability of tailoring the optomechanical coupling of our platform, which can be used in complement to the previously demonstrated control of the relative (dispersive to dissipative) coupling strength via the geometry of the integrated access waveguide.

Collaborative consumption is currently lauded by a number of economists and sections of the media, who extol its many social and environmental merits. It can be defined as the consumerist aspect of the functional economy, its natural extension to the Business-to-Consumer (BtoC) and Consumer-to-Consumer (CtoC) sectors. This article explores this notion of new consumption and examines how it interrelates with and can contribute to the functional economy to develop sustainability. It is based on an analysis of 27 collaborative consumption websites and blogs, together with several academic studies carried out in the field of shared use services. The article studies the reasons and motives that the literature identifies as being used to promote the use of these collaborative services to consumers, and clarifies their contribution and their limits with regard to sustainable consumption.