Wurtzite phase control for self-assisted GaAs nanowires grown by molecular beam epitaxy.

The accurate control of the crystal phase in III-V semiconductor nanowires (NWs) is an important milestone for device applications. Although cubic zinc-blende (ZB) GaAs is a well-established material in microelectronics, the controlled growth of hexagonal wurtzite (WZ) GaAs has thus far not been achieved successfully. Specifically, the prospect of growing defect-free and gold catalyst-free wurtzite GaAs would pave the way towards integration on silicon substrate and new device applications. In this article, we present a method to select and maintain the WZ crystal phase in self-assisted NWs by molecular beam epitaxy. By choosing a specific regime where the NW growth process is a self-regulated system, the main experimental parameter to select the ZB or WZ phase is the V/III flux ratio. Using an analytical growth model, we show that the V/III flux ratio can be finely tuned by changing the As flux, thus driving the system toward a stationary regime where the wetting angle of the Ga droplet can be maintained in the range of values allowing the formation of pure WZ phase. The analysis of the in situ reflection high energy electron diffraction evolution, combined with high-resolution scanning transmission electron microscopy (TEM), dark field TEM, and photoluminescence all confirm the control of an extended pure WZ segment, more than a micrometer long, obtained by molecular beam epitaxy growth of self- assisted GaAs NWs with a V/III flux ratio of 4.0. This successful controlled growth of WZ GaAs suggests potential benefits for electronics and opto-electronics applications.

Fabrication of self-rolling geodesic objects and photonic crystal tubes.

This paper presents a stress engineering method that allows the design and fabrication of the analogs of single-wall nanotubes in the class of photonic crystals. The macroscopic shape of the final object is obtained through the stress relaxation of a pre-stressed multilayer planar design. We illustrate the extent of the proposed method by various single-layer and multilayer photonic crystals tubes and micron-scale objects with 5-fold symmetry.

Crystal phase engineering of self-catalyzed GaAs nanowires using a RHEED diagram.

It is well known that the crystalline structure of the III-V nanowires (NWs) is mainly controlled by the wetting contact angle of the catalyst droplet which can be tuned by the III and V flux. In this work we present a method to control the wurtzite (WZ) or zinc-blende (ZB) structure in self-catalyzed GaAs NWs grown by molecular beam epitaxy, using in situ reflection high energy electron diffraction (RHEED) diagram analysis. Since the diffraction patterns of the ZB and WZ structures differ according to the azimuth [11̄0], it is possible to follow the evolution of the intensity of specific ZB and WZ diffraction spots during NW growth as a function of the growth parameters such as the Ga flux. By analyzing the evolution of the WZ and ZB spot intensities during NW growth with specific changes of the Ga flux, it is then possible to control the crystal structure of the NWs. ZB GaAs NWs with a controlled WZ segment have thus been realized. Using a semi-empirical model for the NW growth and our in situ RHEED measurements, the critical wetting angle of the Ga catalyst droplet for the structural transition is deduced.

Abnormal WNT5A Signaling Causes Mandibular Hypoplasia in Robinow Syndrome.

The study of rare genetic diseases provides valuable insights into human gene function. Here, we investigate dominant Robinow syndrome (RS), which affects the WNT5A signaling pathway. Autosomal dominant RS is caused by missense mutations in WNT5A or nonsense mutations in the adaptor protein DVL1 or DVL3. The recessive form of the disease is caused by loss-of-function mutations in the receptor ROR2. RS is characterized by hypertelorism, midface, and mandibular hypoplasia. Here, we focus on the missense mutations in WNT5A, since the impact on function is difficult to predict from in silico analysis. We used chicken embryo to express wild-type or 2 mutant versions of human WNT5A in the mandible and then examined the morphologic, cellular, and molecular effects. The 3 experimental viruses-wt WNT5A, WNT5AC83S, or WNT5AC182R-all caused shortening of the mandible on the injected side as compared with GFP controls. Although the phenotypes initially appeared similar, we uncovered specific disruption of chondrocyte polarity and shape, inhibition of cell migration, differences in target gene expression, and absence of JNK signaling only in the presence of mutant viruses. In addition, the missense mutations do not appear to block receptor binding, since in paracrine experiments, the mutant protein inhibits cell migration. In this study, we ruled out a straightforward gain or loss of function caused by the WNT5A missense mutations. Instead, the mutations are likely redirecting WNT signaling away from JNK-PCP toward other noncanonical pathways. We conclude that in RS, WNT5A missense mutations have dominant neomorphic effects that interfere with the function of the wild-type protein.