We have investigated for the first time the impact of electron overflow on the performance of nanowire light-emitting diodes (LEDs) operating in the entire visible spectral range, wherein intrinsic white light emission is achieved from self-organized InGaN quantum dots embedded in defect-free GaN nanowires on a single chip. Through detailed temperature-dependent electroluminescence and simulation studies, it is revealed that electron leakage out of the device active region is primarily responsible for efficiency degradation in such nanowire devices, which in conjunction with the presence of nonradiative surface recombination largely determines the unique emission characteristics of nanowire light-emitting diodes. We have further demonstrated that electron overflow in nanowire LEDs can be effectively prevented with the incorporation of a p-doped AlGaN electron blocking layer, leading to the achievement of phosphor-free white light-emitting diodes that can exhibit for the first time virtually zero efficiency droop for injection currents up to ~2200 A/cm(2). This study also provides unambiguous evidence that Auger recombination is not the primary mechanism responsible for efficiency droop in GaN-based nanowire light-emitting diodes.
We have examined the carrier injection process of axial nanowire light-emitting diode (LED) structures and identified that poor carrier injection efficiency, due to the large surface recombination, is the primary cause for the extremely low output power of phosphor-free nanowire white LEDs. We have further developed InGaN/GaN/AlGaN dot-in-a-wire core-shell white LEDs on Si substrate, which can break the carrier injection efficiency bottleneck, leading to a massive enhancement in the output power. At room temperature, the devices can exhibit an output power of ~1.5 mW, which is more than 2 orders of magnitude stronger than nanowire LEDs without shell coverage. Additionally, such phosphor-free nanowire white LEDs can deliver an unprecedentedly high color rendering index of ~92-98 in both the warm and cool white regions, with the color rendering capability approaching that of an ideal light source, i.e. a blackbody.
DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA such as enhancers and promoters; however, the factors affecting the establishment and maintenance of these sites are not fully understood. We now show that HMGN1 and HMGN2, nucleosome-binding proteins that are ubiquitously expressed in vertebrate cells, maintain the DHS landscape of mouse embryonic fibroblasts (MEFs) synergistically. Loss of one of these HMGN variants led to a compensatory increase of binding of the remaining variant. Genome-wide mapping of the DHSs in Hmgn1 −/− , Hmgn2 −/− , and Hmgn1 −/− n2 −/− MEFs reveals that loss of both, but not a single HMGN variant, leads to significant remodeling of the DHS landscape, especially at enhancer regions marked by H3K4me1 and H3K27ac. Loss of HMGN variants affects the induced expression of stress-responsive genes in MEFs, the transcription profiles of several mouse tissues, and leads to altered phenotypes that are not seen in mice lacking only one variant. We conclude that the compensatory binding of HMGN variants to chromatin maintains the DHS landscape, and the transcription fidelity and is necessary to retain wildtype phenotypes. Our study provides insight into mechanisms that maintain regulatory sites in chromatin and into functional compensation among nucleosome binding architectural proteins. [Supplemental material is available for this article.]Tissue-and developmental-specific gene expression is facilitated by the binding of transcription factors to unique DNA sequences at regulatory sites in chromatin, such as enhancers and promoters. At these sites, the organization of the nucleosomes is altered, rendering the DNA more accessible to regulatory factors and hypersensitive to digestion by various nucleases including DNase I. DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA and are used to identify regulatory sites in chromatin. The DHSs chromatin landscape is cell-type specific and dynamic, reflecting changes in the cellular transcription profile occurring during development, or as a consequence of genomic changes leading to altered cellular phenotypes (Gross and Garrard 1988;Boyle et al. 2008;Thurman et al. 2012;Calo and Wysocka 2013;Stergachis et al. 2013).The molecular mechanisms that establish and maintain DHSs and their role in gene expression are key questions in chromatin biology. DHSs are established by the combined action of transcription factors that bind dynamically to specific DNA sequences and 12 These authors contributed equally to this work.
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