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International audience; Significant efforts are currently deployed in order to find optimum GaN-on-silicon epitaxial structuresenabling outstanding DC performances beyond 1 kV while delivering low trapping effects. We report on thedevelopment of GaN-on-silicon heterostructures, designed and manufactured by the company EpiGaNtargeting 1200 V power applications. In particular, it is shown that the insertion of superlattices (SL) into thebuffer layers allows pushing the vertical breakdown voltage above 1200 V without generating additionaltrapping effects as compared to a more standard step-graded AlGaN-based epi-structure using similar totalbuffer thickness. DC characterizations by means of back-gating measurements of fabricated transistorsreflect both the enhancement of the breakdown voltage and the low trapping effects up to 1200 V. Theseresults show that a proper buffer optimization along with the insertion of SL pave the way to GaN-on-siliconlateral power transistors operating at 1200 V with low on-resistance and low trapping effects.Two buffer layers have been compared: one reference buffer without SL with a total thickness of5.5µm and one SL-based buffer with a total thickness of 5µm. Vertical and lateral breakdown voltages havebeen measured at various temperatures. A vertical breakdown of 1300 V at 0.01 A/cm² is reached for thestructure with SL compared to 1000 V for the more standard structure, even though the latter is slightlythicker. Furthermore, it can be noticed that a low vertical leakage current is observed up to a temperatureof 150°C for the SL heterostructure. The leakage current increase up to 150°C is significantly lower than thereference buffer without SL. Also, the lateral breakdown voltage (floating substrate) is well-above 2000V forboth structures when using large contact distances.The effects of buffer traps have been studied through substrate bias ramp measurements usingvarious sweep rates. The reference heterostructure without SL shows low trapping effect up to 800V with astrong trapping activation starting from 900 V. However, the optimized SL buffer uniformly delivers state-ofthe-art low trapping effects all the way to 1300 V.Electrical characterizations have been realized on 2x50 µm transistors with a gate length of 2 µm forseveral gate-drain distances (GD) for both structures. DC characteristics ID-VD and ID-VG reveal a low leakagecurrent and an excellent pinch-off behavior reflecting the absence of parasitic punch-through effect or gateleakage current. It can be noticed that low static on-state resistance (RON_STATIC) of about 5 mΩ/cm² with agate-drain distance of 5 µm has been obtained. For larger GD, RON_STATIC increases as expected but remains stillbelow 15 mΩ/cm² for a GD = 40 µm for instance. Trapping in the buffer (between the 2DEG and the substrate)can be studied by back-gating operation with high vertical drain-to-substrate potential. In this case, tuningthe transistor / substrate bias conditions allows in turn to distinguish the surface and bulk traps. In the presentstudy, this technique has been applied and fully confirms the low buffer trapping up to 1200 V despite residualsurface traps due to the processing that still needs to be optimized.

International audience; The aim of this work is to investigate the role of the epitaxial structure on the low trapping effects of GaN-on-silicon heterostructures use for power application. Structures with and without superlattices (SL) are analysed. In particular, it is shown that the insertion of SL into the buffer layers allows pushing the vertical breakdown voltage above 1200 V without generating additional trapping effects as compared to a more standard GaN-based epi-structure using similar total buffer thickness. A low trapping effect down to-1.2 kV has been observed with substrate ramp measurements. Indeed, we demonstrated that a structure with SL shows a reduction in the trapping effects with high vertical breakdown.

Sphingolipids are considered to play a key role in protein sorting and membrane trafficking. In melanocytic cells, sorting of lysosomal and melanosomal proteins requires the sphingolipid glucosylceramide (GlcCer). This sorting information is located in the lumenal domain of melanosomal proteins. We found that two processes dependent on lumenal pH, protein sialylation and lysosomal acid lipase (LAL) activity were aberrant in GM95 melanocyte cells, which do not produce glycosphingolipids. Using fluorescence lifetime imaging microscopy (FLIM), we found that the lumenal pH in the trans-Golgi network and lysosomes of wild-type melanocyte MEB4 cells are >1 pH unit lower than GM95 cells and fibroblasts. In addition to the lower pH found in vivo, the in vitro activity of the proton pump, the vacuolar-type H+-translocating ATPase (V-ATPase), was twofold higher in MEB4 compared to GM95 cells. The apparent Ki for inhibition of the V-ATPase by concanamycin A and archazolid A, which share a common binding site on the c-ring, was lower in glycosphingolipid-deficient GM95 cells. No difference between the MEB4 and GM95 cells was found for the V-ATPase inhibitors apicularen A and salicylihalimide. We conclude that hyperacidification in MEB4 cells requires glycosphingolipids and propose that low pH is necessary for protein sorting and melanosome biogenesis. Furthermore, we suggest that glycosphingolipids are indirectly involved in protein sorting and melanosome biogenesis by stimulating the proton pump, possibly through binding of GlcCer. These experiments establish, for the first time, a link between pH, glycosphingolipids and melanosome biogenesis in melanocytic MEB4 cells, to suggest a role for glycosphingolipids in hyperacidification in melanocytes.

International audience; Despite superior performance demonstrated by GaN-based power devices [1] as compared to conventional Si-and GaAs-based components, HEMT devices commercialization is still rather limited. This is because the mechanisms such as current collapse, self-heating, strain into the heterostructure, deep traps and surface states still plague the device reliability. Significant improvements have been achieved in GaN technology to efficiently reduce the current collapse, namely by improving the material quality and optimizing proper surface passivation like SiN. However, self-heating and strain relaxation effects strongly affect the device characteristics and result in device degradation [2]. Therefore, investigation and enhancement of the thermal stability of GaN devices are desirable for higher reliability. In this work, the thermal stability of strained AlGaN/GaN, AlN/GaN and unstrained InAlN/GaN heterostructures on low cost Si substrates are compared for the first time. Two-dimensional electron gas (2DEG) channel and Schottky contacts degradation have been studied by high temperature storage tests up to 900°C for various GaN-based configurations. In order to overcome the problem of gate degradation at high temperature, a novel MOSHEMT by means of a thermally grown oxide is proposed for both exponential gate leakage reduction and thermal stability enhancement.

UDP-galactose reaches the Golgi lumen through the UDP-galactose transporter (UGT) and is used for the galactosylation of proteins and lipids. Ceramides and diglycerides are galactosylated within the endoplasmic reticulum by the UDP-galactose: ceramide galactosyltransferase. It is not known how UDP-galactose is transported from the cytosol into the endoplasmic reticulum. We transfected ceramide galactosyltransferase cDNA into CHOlec8 cells, which have a defective UGT and no endogenous ceramide galactosyltransferase. Cotransfection with the human UGT1 greatly stimulated synthesis of lactosylceramide in the Golgi and of galactosylceramide in the endoplasmic reticulum. UDP-galactose was directly imported into the endoplasmic reticulum because transfection with UGT significantly enhanced synthesis of galactosylceramide in endoplasmic reticulum membranes. Subcellular fractionation and double label immunofluorescence microscopy showed that a sizeable fraction of ectopically expressed UGT and ceramide galactosyltransferase resided in the endoplasmic reticulum of CHOlec8 cells. The same was observed when UGT was expressed in human intestinal cells that have an endogenous ceramide galactosyltransferase. In contrast, in CHOlec8 singly transfected with UGT 1, the transporter localized exclusively to the Golgi complex. UGT and ceramide galactosyltransferase were entirely detergent soluble and form a complex because they could be coimmunoprecipitated. We conclude that the ceramide galactosyltransferase ensures a supply of UDP-galactose in the endoplasmic reticulum lumen by retaining UGT in a molecular complex.

In higher eukaryotes, glucosylceramide is the simplest member and precursor of a fascinating class of membrane lipids, the glycosphingolipids. These lipids display an astounding variation in their carbohydrate head groups, suggesting that glycosphingolipids serve specialized functions in recognition processes. It is now realized that they are organized in signalling domains on the cell surface. They are of vital importance as, in their absence, embryonal development is inhibited at an early stage. Remarkably, individual cells can live without glycolipids, perhaps because their survival does not depend on glycosphingolipid–mediated signalling mechanisms. Still, these cells suffer from defects in intracellular membrane transport. Various membrane proteins do not reach their intracellular destination, and, indeed, some intracellular organelles do not properly differentiate to their mature stage. The fact that glycosphingolipids are required for cellular differentiation suggests that there are human diseases resulting from defects in glycosphingolipid synthesis. In addition, the same cellular differentiation processes may be affected by defects in the degradation of glycosphingolipids. At the cellular level, the pathology of glycosphingolipid storage diseases is not completely understood. Cell biological studies on the intracellular fate and function of glycosphingolipids may open new ways to understand and defeat not only lipid storage diseases, but perhaps other diseases that have not been connected to glycosphingolipids so far.

A;lthough glycosphingolipids are ubiquitously expressed and essential for multicellular organisms, surprisingly little is known about their intracellular functions. To explore the role of glycosphingolipids in membrane transport, we used the glycosphingolipid-deficient GM95 mouse melanoma cell line. We found that GM95 cells do not make melanin pigment because tyrosinase, the first and rate-limiting enzyme in melanin synthesis, was not targeted to melanosomes but accumulated in the Golgi complex. However, tyrosinase-related protein 1 still reached melanosomal structures via the plasma membrane instead of the direct pathway from the Golgi. Delivery of lysosomal enzymes from the Golgi complex to endosomes was normal, suggesting that this pathway is not affected by the absence of glycosphingolipids. Loss of pigmentation was due to tyrosinase mislocalization, since transfection of tyrosinase with an extended transmembrane domain, which bypassed the transport block, restored pigmentation. Transfection of ceramide glucosyltransferase or addition of glucosylsphingosine restored tyrosinase transport and pigmentation. We conclude that protein transport from Golgi to melanosomes via the direct pathway requires glycosphingolipids.