Spin defects in silicon carbide have exceptional electron spin coherence with a nearinfrared spin-photon interface in a material amenable to modern semiconductor fabrication. Leveraging these advantages, we successfully integrate highly coherent single neutral divacancy spins in commercially available p-i-n structures and fabricate diodes to modulate the local electrical environment of the defects. These devices enable deterministic charge state control and broad Stark shift tuning exceeding 850 GHz. Surprisingly, we show that charge depletion results in a narrowing of the optical linewidths by over 50 fold, approaching the lifetime limit. These results demonstrate a method for mitigating the ubiquitous problem of spectral diffusion in solid-state emitters by engineering the electrical environment while utilizing classical semiconductor devices to control scalable spin-based quantum systems.

Hybrid spin-mechanical systems provide a platform for integrating quantum registers and transducers. Efficient creation and control of such systems require a comprehensive understanding of the individual spin and mechanical components as well as their mutual interactions. Point defects in silicon carbide (SiC) offer long-lived, optically addressable spin registers in a wafer-scale material with low acoustic losses, making them natural candidates for integration with high quality factor mechanical resonators. Here, we show Gaussian focusing of a surface acoustic wave in SiC, characterized by a novel stroboscopic X-ray diffraction imaging technique, which delivers direct, strain amplitude information at nanoscale spatial resolution. Using ab initio calculations, we provide a more complete picture of spin-strain coupling for various defects in SiC with C 3v symmetry. This reveals the importance of shear for future device engineering and enhanced spin-mechanical coupling. We demonstrate all-optical detection of acoustic paramagnetic resonance without microwave magnetic fields, relevant to sensing applications. Finally, we show mechanically driven Autler-Townes splittings and magnetically forbidden Rabi oscillations. These results offer a basis for full strain control of three-level spin systems.

Defects in silicon carbide (SiC) have emerged as a favorable platform for optically active spin-based quantum technologies. Spin qubits exist in specific charge states of these defects, where the ability to control these states can provide enhanced spin-dependent readout and long-term charge stability. We investigate this charge state control for two major spin qubits in 4H-SiC, the divacancy and silicon vacancy, obtaining bidirectional optical charge conversion between the bright and dark states of these defects. We measure increased photoluminescence from divacancy ensembles by up to three orders of magnitude using near-ultraviolet excitation, depending on the substrate, and without degrading the electron spin coherence time. This charge conversion remains stable for hours at cryogenic temperatures, allowing spatial and persistent patterning of the charge state populations. We develop a comprehensive model of the defects and optical processes involved, offering a strong basis to improve material design and to develop quantum applications in SiC.

Defects with associated electron and nuclear spins in solid-state materials have a long history relevant to quantum information science going back to the first spin echo experiments with silicon dopants in the 1950s. Since the turn of the century, the field has rapidly spread to a vast array of defects and host crystals applicable to quantum communication, sensing, and computing. From simple spin resonance to longdistance remote entanglement, the complexity of working with spin defects is fast advancing, and requires an in-depth understanding of their spin, optical, charge, and material properties in this modern context. This is especially critical for discovering new relevant systems dedicated to specific quantum applications. In this review, we therefore expand upon all the key components with an emphasis on the properties of defects and the host material, on engineering opportunities and other pathways for improvement. Finally, this review aims to be as defect and material agnostic as possible, with some emphasis on optical emitters, providing a broad guideline for the field of solid-state spin defects for quantum information.

The ataxia (ax J ) mutation is a spontaneous recessive mutation that results in reduced expression of ubiquitinspecific protease 14, Usp14. Mice homozygous for the ax J mutation are retarded for growth and exhibit several behavioral disorders, including a resting tremor and hindlimb paralysis. Although pathological defects appear to be limited to the central nervous system, reduction of Usp14 expression was widespread in the ax J mice. Usp14 co-fractionated with proteasomes isolated from livers and brains of wildtype mice. Proteasomes isolated from the ax J brains still possessed deubiquitinating activity and were functionally competent to hydrolyze 20S proteasomal substrates in vitro. However, the levels of monomeric ubiquitin were reduced approximately 35% in most of the ax J tissues examined.These results indicate that Usp14 functions to maintain the cellular levels of monomeric ubiquitin in mammalian cells, and that alterations in the levels of ubiquitin may contribute to neurological disease. Keywords: ataxia, mutation, neurological, proteasome, ubiquitin, ubiquitin-specific protease 14. . These disorders are associated with changes in protein degradation that are manifested through the production of protein aggregates. However, it is unclear whether these alterations in the UPS are the primary cause or a secondary consequence of these disorders. Our recent studies on ataxia (ax J ) mice indicate that primary alterations in the UPS can lead to neurological dysfunction (Wilson et al. 2002). The ax J mutation is a spontaneously arising recessive neurological mutation (D'Amato and Hicks 1965). The ax J mice suffer from progressive motor system abnormalities that first appear as a resting tremor when the mice are 2-3 weeks old. At 4 weeks of age, ax J mice exhibit severe hind muscle wasting and ataxia. These mice are completely immobile by 6 weeks of age and death occurs at about 8 weeks of age. The neurological phenotypes observed in the ax J mice are the result of a genetic lesion in the gene encoding the deubiquitinating enzyme Usp14 (Wilson et al. 2002). The insertion of an intracisternal A-particle into intron 5 of Usp14 reduces the expression of Usp14 in the ax J mice to only 5-10% of the levels found in wild-type mice, indicating that the ax J mutation represents a hypomorphic allele of Usp14. A better understanding of the deficiencies in the ax J mice, and in other mice that harbor mutations in the UPS, should therefore provide valuable insights into how the UPS functions in the nervous system and how alterations in these pathways lead to disease.

Solid-state quantum emitters with spin registers are promising platforms for quantum communication, yet few emit in the narrow telecom band necessary for low-loss fiber networks. Here, we create and isolate near-surface single vanadium dopants in silicon carbide (SiC) with stable and narrow emission in the O band, with brightness allowing cavity-free detection in a wafer-scale material. In vanadium ensembles, we characterize the complex d1 orbital physics in all five available sites in 4H-SiC and 6H-SiC. The optical transitions are sensitive to mass shifts from local silicon and carbon isotopes, enabling optically resolved nuclear spin registers. Optically detected magnetic resonance in the ground and excited orbital states reveals a variety of hyperfine interactions with the vanadium nuclear spin and clock transitions for quantum memories. Last, we demonstrate coherent quantum control of the spin state. These results provide a path for telecom emitters in the solid state for quantum applications.

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Estrogen replacement therapy appears to delay the onset of Alzheimer's disease (AD), but the mechanisms for this action are incompletely known. We show how the enhancement of synaptic sprouting by estradiol (E 2 ) in response to an entorhinal cortex (EC) lesion model of AD may operate via an apolipoprotein E (apoE)-dependent mechanism. In wild-type (WT) mice, ovariectomy decreased commissural/associational sprouting to the inner molecular layer of the dentate gyrus, with synaptophysin (SYN) as a marker. E 2 replacement returned SYN in the inner layer to levels of EC-lesioned, ovary-bearing controls and increased the area of compensatory synaptogenesis in the outer molecular layer. In EC-lesioned apoE-knock-out (KO) mice, however, E 2 did not enhance sprouting. We also examined apoJ (clusterin) mRNA, which is implicated in AD by its presence in senile plaques, its transport of A␤ across the blood-brain barrier, and its induction by neurodegenerative lesioning. ApoJ mRNA levels were increased by E 2 replacement in EC-lesioned WT mice but not in apoE-KO mice. These data suggest a mechanism for the protective effects of estrogens on AD and provide a link between two important risk factors in the etiology of AD, the apoE ⑀4 genotype and an estrogen-deficient state. This is also the first evidence that SYN, a presynaptic protein involved in neurotransmitter release, is regulated by E 2 in the adult brain, and that apoE is necessary for the induction of apoJ mRNA by E 2 in brain injury.