Encoding multistate charge order and chirality in endotaxial heterostructures

Intrinsic resistivity changes associated with charge density wave (CDW) phase transitions in 1T-TaS$_2$ hold promise for non-volatile memory and computing devices based on the principle of phase change memory (PCM). High-density PCM storage is proposed for materials with multiple intermediate resistance states, which have been observed in 1T-TaS$_2$. However, the metastability responsible for this behavior makes the presence of multistate switching unpredictable in 1T-TaS$_2$ devices. Here, we demonstrate the synthesis of nanothick verti-lateral 1H-TaS$_2$/1T-TaS$_2$ heterostructures in which the number of endotaxial metallic 1H-TaS$_2$ monolayers dictates the number of high-temperature resistance transitions in 1T-TaS$_2$ lamellae. Further, we also observe optically active heterochirality in the CDW superlattice structure, which is modulated in concert with the resistivity steps. This thermally-induced polytype conversion nucleates at folds and kinks where interlayer translations that relax local strain favorably align 1H and 1T layers. This work positions endotaxial TaS$_2$ heterostructures as prime candidates for non-volatile device schemes implementing coupled switching of structure, chirality, and resistance

The laurentian record of neoproterozoic glaciation, tectonism, and eukaryotic evolution in Death Vally, California

Neoproterozoic strata in Death Valley, California contain eukaryotic microfossils and glacial deposits that have been used to assess the severity of putative Snowball Earth events and the biological response to extreme environmental change. These successions also contain evidence for syn-sedimentary faulting that has been related to the rifting of Rodinia, and in turn the tectonic context of the onset of Snowball Earth. These interpretations hinge on local geological relationships and both regional and global stratigraphic correlations. Here we present new geological mapping, measured stratigraphic sections, carbon and strontium isotope chemostratigraphy, and micropaleontology from the Neoproterozoic glacial deposits and bounding strata in Death Valley. These new data enable us to refine regional correlations both across Death Valley and throughout Laurentia, and construct a new age model for glaciogenic strata and microfossil assemblages. Particularly, our remapping of the Kingston Peak Formation in the Saddle Peak Hills and near the type locality shows for the first time that glacial deposits of both the Marinoan and Sturtian glaciations can be distinguished in southeastern Death Valley, and that beds containing vase-shaped microfossils are slump blocks derived from the underlying strata. These slump blocks are associated with multiple overlapping unconformities that developed during syn-sedimentary faulting, which is a common feature of Cyrogenian strata along the margin of Laurentia from California to Alaska. With these data, we conclude that all of the microfossils that have been described to date in Neoproterozoic strata of Death Valley predate the glaciations and do not bear on the severity, extent or duration of Neoproterozoic Snowball Earth events

Spontaneous supercrystal formation during a strain-engineered metal-insulator transition

Mott metal-insulator transitions possess electronic, magnetic, and structural degrees of freedom promising next generation energy-efficient electronics. We report a previously unknown, hierarchically ordered state during a Mott transition and demonstrate correlated switching of functional electronic properties. We elucidate in-situ formation of an intrinsic supercrystal in a Ca2RuO4 thin film. Machine learning-assisted X-ray nanodiffraction together with electron microscopy reveal multi-scale periodic domain formation at and below the film transition temperature (TFilm ~ 200-250 K) and a separate anisotropic spatial structure at and above TFilm. Local resistivity measurements imply an intrinsic coupling of the supercrystal orientation to the material's anisotropic conductivity. Our findings add an additional degree of complexity to the physical understanding of Mott transitions, opening opportunities for designing materials with tunable electronic properties

Cooperativity between the preproinsulin mRNA untranslated regions Is necessary for glucose-stimulated translation

Glucose regulates proinsulin biosynthesis via stimulation of the translation of the preproinsulin mRNA in pancreatic β-cells. However, the mechanism by which this occurs has remained unclear. Using recombinant adenoviruses that express the preproinsulin mRNA with defined alterations, the untranslated regions (UTRs) of the preproinsulin mRNA were examined for elements that specifically control translation of the mRNA in rat pancreatic islets. These studies revealed that the preproinsulin 5′-UTR was necessary for glucose stimulation of preproinsulin mRNA translation, whereas the 3′-UTR appeared to suppress translation. However, together the 5′- and 3′-UTRs acted cooperatively to markedly increase glucose-induced proinsulin biosynthesis. In primary hepatocytes the presence of the preproinsulin 3′-UTR led to reduced mRNA levels compared with the presence of the SV40 3′-UTR, consistent with the presence of mRNA stability determinants in the 3′-UTR that stabilize the preproinsulin mRNA in a pancreatic β-cell-specific manner. Translation of these mRNAs in primary hepatocytes was not stimulated by glucose, indicating that regulated translation of the preproinsulin mRNA occurs in a pancreatic β-cell-specific manner. Thus, the untranslated regions of the preproinsulin mRNA play crucial roles in regulating insulin production and therefore glucose homeostasis by regulating the translation and the stability of the preproinsulin mRNA

Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis

Heterozygous coding mutations in the INS gene that encodes preproinsulin were recently shown to be an important cause of permanent neonatal diabetes. These dominantly acting mutations prevent normal folding of proinsulin, which leads to beta-cell death through endoplasmic reticulum stress and apoptosis. We now report 10 different recessive INS mutations in 15 probands with neonatal diabetes. Functional studies showed that recessive mutations resulted in diabetes because of decreased insulin biosynthesis through distinct mechanisms, including gene deletion, lack of the translation initiation signal, and altered mRNA stability because of the disruption of a polyadenylation signal. A subset of recessive mutations caused abnormal INS transcription, including the deletion of the C1 and E1 cis regulatory elements, or three different single base-pair substitutions in a CC dinucleotide sequence located between E1 and A1 elements. In keeping with an earlier and more severe beta-cell defect, patients with recessive INS mutations had a lower birth weight (-3.2 SD score vs. -2.0 SD score) and were diagnosed earlier (median 1 week vs. 10 weeks) compared to those with dominant INS mutations. Mutations in the insulin gene can therefore result in neonatal diabetes as a result of two contrasting pathogenic mechanisms. Moreover, the recessively inherited mutations provide a genetic demonstration of the essential role of multiple sequence elements that regulate the biosynthesis of insulin in man

Insulin Gene Expression Is Regulated by DNA Methylation

BACKGROUND:Insulin is a critical component of metabolic control, and as such, insulin gene expression has been the focus of extensive study. DNA sequences that regulate transcription of the insulin gene and the majority of regulatory factors have already been identified. However, only recently have other components of insulin gene expression been investigated, and in this study we examine the role of DNA methylation in the regulation of mouse and human insulin gene expression. METHODOLOGY/PRINCIPAL FINDINGS:Genomic DNA samples from several tissues were bisulfite-treated and sequenced which revealed that cytosine-guanosine dinucleotide (CpG) sites in both the mouse Ins2 and human INS promoters are uniquely demethylated in insulin-producing pancreatic beta cells. Methylation of these CpG sites suppressed insulin promoter-driven reporter gene activity by almost 90% and specific methylation of the CpG site in the cAMP responsive element (CRE) in the promoter alone suppressed insulin promoter activity by 50%. Methylation did not directly inhibit factor binding to the CRE in vitro, but inhibited ATF2 and CREB binding in vivo and conversely increased the binding of methyl CpG binding protein 2 (MeCP2). Examination of the Ins2 gene in mouse embryonic stem cell cultures revealed that it is fully methylated and becomes demethylated as the cells differentiate into insulin-expressing cells in vitro. CONCLUSIONS/SIGNIFICANCE:Our findings suggest that insulin promoter CpG demethylation may play a crucial role in beta cell maturation and tissue-specific insulin gene expression

The Future of the Correlated Electron Problem

The understanding of material systems with strong electron-electron interactions is the central problem in modern condensed matter physics. Despite this, the essential physics of many of these materials is still not understood and we have no overall perspective on their properties. Moreover, we have very little ability to make predictions in this class of systems. In this manuscript we share our personal views of what the major open problems are in correlated electron systems and we discuss some possible routes to make progress in this rich and fascinating field. This manuscript is the result of the vigorous discussions and deliberations that took place at Johns Hopkins University during a three-day workshop January 27, 28, and 29, 2020 that brought together six senior scientists and 46 more junior scientists. Our hope, is that the topics we have presented will provide inspiration for others working in this field and motivation for the idea that significant progress can be made on very hard problems if we focus our collective energies.Comment: 55 pages, 19 figure

Tectonic model for development of the Byrd Glacier discontinuity and surrounding regions of the Transantarctic Mountains during Neoproterozoic-Early Paleozoic

The Byrd Glacier discontinuity us a major boundary crossing the Ross Orogen, with crystalline rocks to the north and primarily sedimentary rocks to the south. Most models for the tectonic development of the Ross Orogen in the central Transantarctic Mountains consits of two-dimensional transects across the belt, but do not adress the major longitudinal contrast at Byrd Glacier. This paper presents a tectonic model centering on the Byrd Glacier discontinuity. Rifting in the Neoproterozoic producede a crustal promontory in the craton margin to the north of Byrd Glacier. Oblique convergence of the terrane (Beardmore microcontinent) during the latest Neroproterozoic and Early Cambrian was accompanied by subduction along the craton margin of East Antarctica. New data presented herein in the support of this hypothesis are U-Pb dates of 545.7 ± 6.8 Ma and 531.0 ± 7.5 Ma on plutonic rocks from the Britannia Range, subduction stepped out, and Byrd Glacier. After docking of the terrane, subduction stepped out, and Byrd Group was deposited during the Atdabanian-Botomian across the inner margin of the terrane. Beginning in the upper Botomian, reactivation of the sutured boundaries of the terrane resulted in an outpouring of clastic sediment and folding and faulting of the Byrd Group