New signatures of the spin gap in quantum point contacts.

One dimensional semiconductor systems with strong spin-orbit interaction are both of fundamental interest and have potential applications to topological quantum computing. Applying a magnetic field can open a spin gap, a pre-requisite for Majorana zero modes. The spin gap is predicted to manifest as a field dependent dip on the first 1D conductance plateau. However, disorder and interaction effects make identifying spin gap signatures challenging. Here we study experimentally and numerically the 1D channel in a series of low disorder p-type GaAs quantum point contacts, where spin-orbit and hole-hole interactions are strong. We demonstrate an alternative signature for probing spin gaps, which is insensitive to disorder, based on the linear and non-linear response to the orientation of the applied magnetic field, and extract a spin-orbit gap ΔE ≈ 500 µeV. This approach could enable one-dimensional hole systems to be developed as a scalable and reproducible platform for topological quantum applications.

Detection and Control of Spin-Orbit Interactions in a GaAs Hole Quantum Point Contact.

We investigate the relationship between the Zeeman interaction and the inversion-asymmetry-induced spin-orbit interactions (Rashba and Dresselhaus SOIs) in GaAs hole quantum point contacts. The presence of a strong SOI results in the crossing and anticrossing of adjacent spin-split hole subbands in a magnetic field. We demonstrate theoretically and experimentally that the anticrossing energy gap depends on the interplay between the SOI terms and the highly anisotropic hole g tensor and that this interplay can be tuned by selecting the crystal axis along which the current and magnetic field are aligned. Our results constitute the independent detection and control of the Dresselhaus and Rashba SOIs in hole systems, which could be of importance for spintronics and quantum information applications.

Carrier screening for cystic fibrosis in US genetic testing laboratories: a survey of laboratory directors.

Initial guidelines for cystic fibrosis (CF) carrier screening were issued in 2001 by the American College of Medical Genetics and the American College of Obstetricians and Gynecologists and updated in 2004. It is unknown how these guidelines have influenced laboratory practice. This study examined the uptake of two components of these guidelines for CF screening in genetic testing laboratories. A survey of directors of US genetic testing laboratories was conducted. Of 190 respondents, 178 answered questions about CF testing. Nearly half (49%) performed some type of DNA testing for CF; most of these (92%) performed CF carrier screening. Ten percent used a 23-mutation panel for CF screening. The results of 5T tests were reported as a reflex test by 79% of laboratories, while 8% always returned 5T results and 7% never returned them. Seven percent of laboratories adopted both guidelines, 80% adopted one of the two guidelines, and 13% had not adopted either recommendation, suggesting that factors other than clinical guidelines may influence laboratories' CF screening practices. Further studies are needed to determine whether the adoption of CF screening guidelines has significant clinical or economic effects on population-based CF screening programs.

Dominant and recessive mutations define functional domains of Toll, a transmembrane protein required for dorsal-ventral polarity in the Drosophila embryo.

The asymmetry of the dorsal-ventral pattern of the Drosophila embryo appears to depend on the ventral activation of the transmembrane Toll protein. The Toll protein is found around the entire dorsal-ventral circumference of the embryo, and it appears to act as a receptor for a ventral, extracellular signal and to then relay that signal to the cytoplasm in ventral regions of the embryo. Three of five recessive loss-of-function alleles of Toll are caused by point mutations in the region of the cytoplasmic domain of Toll that is similar to the mammalian interleukin-1 receptor, supporting the hypothesis that Toll acts as a signal-transducing receptor. Nine dominant gain-of-function alleles that cause Toll to be active in dorsal, as well as ventral, regions of the embryo are caused by mutations in the extracellular domain. Three of the dominant alleles appear to cause the protein to be constitutively active and are caused by cysteine-to-tyrosine changes immediately outside the transmembrane domain. All six of the remaining dominant alleles require the presence of a wild-type transmembrane Toll protein for their ventralizing effect and all encode truncated proteins that lack the transmembrane and cytoplasmic domains.

The Toll gene of Drosophila, required for dorsal-ventral embryonic polarity, appears to encode a transmembrane protein.

The Toll gene of Drosophila, a maternal effect gene that plays a central role in the establishment of the embryonic dorsal-ventral pattern, has been cloned using P element tagging. A 5.3 kb poly(A)+ ovarian transcript from the cloned region was purified by hybrid selection with the cloned DNA. This purified transcript complements the Toll mutant phenotype when injected into Toll- embryos, which proves that it is the Toll transcript. The sequence of cDNAs suggests that the Toll protein is an integral membrane protein with a cytoplasmic domain and a large extracytoplasmic domain. The putative extracytoplasmic domain contains at least 15 repeats of a 24 amino acid, leucine-rich sequence found in both human and yeast membrane proteins.