Improved performance of InGaN-based red light-emitting diodes by micro-hole arrays.

This study demonstrates the performance improvements of InGaN-based red light-emitting diodes (LEDs) by fabricating micro-holes in the planar mesa. The peak wavelengths of the micro-hole LEDs (MHLEDs) exhibited a blue-shift of around 3 nm compared to the planar LEDs (PLEDs) at the same current density. The lowest full width at half maximum of MHLEDs was 59 nm, which is slightly less than that of the PLEDs. The light output power and external quantum efficiency of the MHLED with a wavelength of 634 nm at 20 mA were 0.6 mW and 1.5%, which are 8.5% higher than those of the PLED.

Optimal ITO transparent conductive layers for InGaN-based amber/red light-emitting diodes.

Fabrication of indium tin oxide (ITO) was optimized for InGaN-based amber/red light-emitting diodes (LEDs). A radiofrequency sputtering reduced the sheet resistivity of ITO at low pressures, and a subsequent two-step annealing resulted in a low sheet resistivity (below 2×10-4 Ωcm) and high transmittance (over 98%) in the amber and red regions between 590 nm to 780 nm. Double ITO layers by sputtering could form an excellent ohmic contact with p-GaN. Application of the double ITO layers on amber and red LEDs enhanced light output power by 15.6% and 13.0%, respectively, compared to those using ITO by e-beam evaporation.

Investigation of N-polar InGaN growth on misoriented ScAlMgO4 substrates.

We report the growth of N-polar InGaN layers on misoriented ScAlMgO4 (SAM) substrates with offset of 0.3 to 5.8° toward the m-plane. The surface of N-polar InGaN with small-offset substrates exhibited hexagonal hillocks similar to those commonly observed in N-polar GaN layers. Larger misorientation angles resulted in smoother surfaces of the InGaN layers. In contrast, the crystalline quality of InGaN indicated an opposite trend with significantly improved quality observed at smaller misorientation angles. We obtained an unprecedented crystalline quality of N-polar InGaN using SAM substrates with a 0.5° offset, which exhibited a [Formula: see text] X-ray rocking curve full width at half maximum value of 223 arcsec. The crystalline quality and surface morphology of InGaN were significantly influenced by the step surface of substrates according to atomic force microscopy observations.

The efficiency of Xenopus primordial germ cell migration depends on the germplasm mRNA encoding the PDZ domain protein Grip2.

A microarray analysis of vegetal pole sequences in the egg and early Xenopus laevis embryo identified Unigene Xl.14891 as a vegetally localized RNA. Analysis of the Xenopus tropicalis genome showed this Unigene to be localized near the 3' end of the Grip2 (glutamate receptor interacting protein 2) transcription unit. RACE showed that the Unigene represented the 3' UTR of Grip2 mRNA. Grip2 mRNA is present in the mitochondrial cloud of late pre-vitellogenic oocytes and then in the germplasm through oogenesis and early development until tailbud tadpole stages. Interference with Grip2 mRNA translation using two antisense morpholino oligos (MOs) impairs primordial germ cell (PGC) migration to the germinal ridges. Both MOs also inhibit swimming movements of the tailbud tadpole, known to involve glutamate receptors. We conclude that Grip2 has several functions in the embryo, including enabling efficient PGC migration.

Liver Specification in the Absence of Cardiac Differentiation Revealed by Differential Sensitivity to Wnt/ß Catenin Pathway Activation.

Embryonic precursors of liver and heart, whilst not sharing cellular origin, develop in close proximity through a dynamic series of inductive signaling events. During gastrulation anterior endoderm (AE) provides cardiogenic signals that act on adjacent mesoderm, resulting in induction of cardiac precursors. Subsequently cardiogenic mesoderm generates a FGF signal that acts on adjacent AE to induce foregut organ specification. Additional signals such as BMP and Wnt provide further information required for liver specification. Most findings on liver specification were derived from mouse explant studies as well as experiments with Xenopus and zebrafish embryos. To address some of the limitations of these models, here we used two complementary ex vivo models based on Xenopus embryos: pluripotent animal cap explants expressing Gata4 transcription factor and conjugates of gastrula-stage AE with animal caps (AC). We show that in these models liver specification is not sensitive to Wnt signaling manipulation, in contrast to the requirement for Wnt antagonism shown in vivo. FGF pathway is not necessary for Gata4-induced liver specification in animal cap explants but is required for prolonged period in sandwiches of AE and AC. In contrast, BMP signaling is shown to be essential for Gata4-induced liver specification. Our findings may have implications for research on liver differentiation from embryonic stem cells.

Carboxy terminus of GATA4 transcription factor is required for its cardiogenic activity and interaction with CDK4.

GATA4-6 transcription factors regulate numerous aspects of development and homeostasis in multiple tissues of mesodermal and endodermal origin. In the heart, the best studied of these factors, GATA4, has multiple distinct roles in cardiac specification, differentiation, morphogenesis, hypertrophy and survival. To improve understanding of how GATA4 achieves its numerous roles in the heart, here we have focused on the carboxy-terminal domain and the residues required for interaction with cofactors FOG2 and Tbx5. We present evidence that the carboxy terminal region composed of amino acids 362-400 is essential for mediating cardiogenesis in Xenopus pluripotent explants and embryos. In contrast, the same region is not required for endoderm-inducing activity of GATA4. Further evidence is presented that the carboxy terminal cardiogenic region of GATA4 does not operate as a generic transcriptional activator. Potential mechanism of action of the carboxy terminal end of GATA4 is provided by the results showing physical and functional interaction with CDK4, including the enhancement of cardiogenic activity of GATA4 by CDK4. These results establish CDK4 as a GATA4 partner in cardiogenesis. The interactions of GATA4 with its other well described cofactors Tbx5 and FOG2 are known to be involved in heart morphogenesis, but their requirement for cardiac differentiation is unknown. We report that the mutations that disrupt interactions of GATA4 with Tbx5 and FOG2, G295S and V217G, respectively, do not impair cardiogenic activity of GATA4. These findings add support to the view that distinct roles of GATA4 in the heart are mediated by different determinants of the protein. Finally, we show that the rat GATA4 likely induces cardiogenesis cell autonomously or directly as it does not require activity of endodermal transcription factor Sox17, a GATA4 target gene that induces cardiogenesis non-cell autonomously.

Transient activation of meox1 is an early component of the gene regulatory network downstream of hoxa2.

Hox genes encode transcription factors that regulate morphogenesis in all animals with bilateral symmetry. Although Hox genes have been extensively studied, their molecular function is not clear in vertebrates, and only a limited number of genes regulated by Hox transcription factors have been identified. Hoxa2 is required for correct development of the second branchial arch, its major domain of expression. We now show that Meox1 is genetically downstream from Hoxa2 and is a direct target. Meox1 expression is downregulated in the second arch of Hoxa2 mouse mutant embryos. In chromatin immunoprecipitation (ChIP), Hoxa2 binds to the Meox1 proximal promoter. Two highly conserved binding sites contained in this sequence are required for Hoxa2-dependent activation of the Meox1 promoter. Remarkably, in the absence of Meox1 and its close homolog Meox2, the second branchial arch develops abnormally and two of the three skeletal elements patterned by Hoxa2 are malformed. Finally, we show that Meox1 can specifically bind the DNA sequences recognized by Hoxa2 on its functional target genes. These results provide new insight into the Hoxa2 regulatory network that controls branchial arch identity.

Six2 functions redundantly immediately downstream of Hoxa2.

Hox transcription factors control morphogenesis along the head-tail axis of bilaterians. Because their direct functional targets are still poorly understood in vertebrates, it remains unclear how the positional information encoded by Hox genes is translated into morphogenetic changes. Here, we conclusively demonstrate that Six2 is a direct downstream target of Hoxa2 in vivo and show that the ectopic expression of Six2, observed in the absence of Hoxa2, contributes to the Hoxa2 mouse mutant phenotype. We propose that Six2 acts to mediate Hoxa2 control over the insulin-like growth factor pathway during branchial arch development.

Global analysis of the transcriptional network controlling Xenopus endoderm formation.

A conserved molecular pathway has emerged controlling endoderm formation in Xenopus zebrafish and mice. Key genes in this pathway include Nodal ligands and transcription factors of the Mix-like paired homeodomain class, Gata4-6 zinc-finger factors and Sox17 HMG domain proteins. Although a linear epistatic pathway has been proposed, the precise hierarchical relationships between these factors and their downstream targets are largely unresolved. Here, we have used a combination of microarray analysis and loss-of-function experiments to examine the global regulatory network controlling Xenopus endoderm formation. We identified over 300 transcripts enriched in the gastrula endoderm, including most of the known endoderm regulators and over a hundred uncharacterized genes. Surprisingly only 10% of the endoderm transcriptome is regulated as predicted by the current linear model. We find that Nodal genes, Mixer and Sox17 have both shared and distinct sets of downstream targets, and that a number of unexpected autoregulatory loops exist between Sox17 and Gata4-6, between Sox17 and Bix1/Bix2/Bix4, and between Sox17 and Xnr4. Furthermore, we find that Mixer does not function primarily via Sox17 as previously proposed. These data provides new insight into the complexity of endoderm formation and will serve as valuable resource for establishing a complete endoderm gene regulatory network.