Interface engineering of 9X stacked 3D NAND flash memory using hydrogen post-treatment annealing.

This study investigates the effects of hydrogen post-treatment on 3D NAND flash memory. Hydrogen post-treatment annealing (PTA) is suggested to passivate the defects in the tunneling oxide/poly-Si interface and inside the poly-Si channel. However, excess hydrogen PTA can release hydrogen atoms from the passivated defects, which may degrade device performance. Therefore, it is important to determine the appropriate PTA condition for optimization of the device performance. Three different conditions for hydrogen PTA, namely Reference, H, and H++, are applied to observe the effects on device performance. The activation energy (Ea) of the device parameters was extracted according to the hydrogen PTA condition to analyze the effects. The extractedEais about 74 meV for Reference, 53 meV for H, and 58 meV for H++conditions, with the best performance observed at the H condition. Optimal hydrogen PTA shows the best on-current (51% higher than Reference) and stable short-term retention (66% suppressedΔVTthan Reference) in 9X stacked 3D NAND flash memory.

Drosophila NSD deletion induces developmental anomalies similar to those seen in Sotos syndrome 1 patients.

BACKGROUND: Haploinsufficiency of the human nuclear receptor binding suppressor of variegation 3-9, enhancer of zeste, and trithorax (SET) domain 1 (NSD1) gene causes a developmental disorder called Sotos syndrome 1 (SOTOS1), which is associated with overgrowth and macrocephaly. NSD family proteins encoding histone H3 lysine 36 (H3K36) methyltransferases are conserved in many species, and Drosophila has a single NSD homolog gene, NSD. OBJECTIVE: To gain insight into the biological functions of NSD1 deficiency in the developmental anomalies seen in SOTOS1 patients using an NSD-deleted Drosophila mutant. METHODS: We deleted Drosophila NSD using CRISPR/Cas9-mediated targeted gene knock-out, and analyzed pleiotropic phenotypes of the homozygous mutant of NSD (NSD-/-) at various developmental stages to understand the roles of NSD in Drosophila. RESULTS: The site-specific NSD deletion was confirmed in the mutant. The H3K36 di-methylation levels were dramatically decreased in the NSD-/- fly. Compared with the control, the NSD-/- fly displayed an increase in the body size of larvae, similar to the childhood overgrowth phenotype of SOTOS1 patients. Although the NSD mutant flies survived to adulthood, their fecundity was dramatically decreased. Furthermore, the NSD-/- fly showed neurological dysfunctions, such as lower memory performance and motor defects, and a diminished extracellular signal-regulated kinase (ERK) activity. CONCLUSIONS: The NSD-deleted Drosophila phenotype resembles many of the phenotypes of SOTOS1 patients, such as learning disability, deregulated ERK signaling, and overgrowth; thus, this mutant fly is a relevant model organism to study various SOTOS1 phenotypes.

The Drosophila histone methyltransferase NSD is positively regulated by the DRE/DREF system.

The Drosophila nuclear receptor-binding SET domain protein (NSD) gene encodes the Drosophila ortholog of mammalian NSD family members that are important in many aspects of development and disease in humans. In this study, we observed that overexpression of Drosophila NSD in imaginal discs induces organ atrophy. Thus, to gain an understanding of the transcriptional regulation of the gene, we analyzed the NSD promoter region. First, we identified the presence of three putative DNA replication-related element (DRE) sequences in its promoter region, where DRE-binding factor (DREF) could bind for transcriptional activation. In the experiments with the fly GAL4-UAS system, we demonstrated that overexpressed DREF increased the endogenous NSD transcription. To confirm the role of DREF as a transcriptional activator on the NSD expression, we generated a series of luciferase reporter gene constructs containing deleted portions of the 5'-flanking regions as well as point mutations in the putative DRE sites. When transiently transfected into S2 cells, the deletion construct containing no DRE sites showed dramatic decrease in the NSD promoter activity, but only two sites near the transcriptional start site were important. Furthermore, we verified the direct interaction of DREF with the two positively cis-acting sequences on the NSD promoter by chromatin immunoprecipitation assay. Taken together, these results demonstrated that NSD is one of the downstream targets of the DRE/DREF pathway that is associated with various cellular processes in Drosophila, indicating that our findings may contribute to the understanding of molecular mechanisms in complex disorders associated with NSD family members in humans.