Search for Dark-Matter-Nucleon Interactions via Migdal Effect with DarkSide-50.

Dark matter elastic scattering off nuclei can result in the excitation and ionization of the recoiling atom through the so-called Migdal effect. The energy deposition from the ionization electron adds to the energy deposited by the recoiling nuclear system and allows for the detection of interactions of sub-GeV/c^{2} mass dark matter. We present new constraints for sub-GeV/c^{2} dark matter using the dual-phase liquid argon time projection chamber of the DarkSide-50 experiment with an exposure of (12 306±184) kg d. The analysis is based on the ionization signal alone and significantly enhances the sensitivity of DarkSide-50, enabling sensitivity to dark matter with masses down to 40 MeV/c^{2}. Furthermore, it sets the most stringent upper limit on the spin independent dark matter nucleon cross section for masses below 3.6 GeV/c^{2}.

Search for Dark Matter Particle Interactions with Electron Final States with DarkSide-50.

We present a search for dark matter particles with sub-GeV/c^{2} masses whose interactions have final state electrons using the DarkSide-50 experiment's (12 306±184) kg d low-radioactivity liquid argon exposure. By analyzing the ionization signals, we exclude new parameter space for the dark matter-electron cross section σ[over ¯]_{e}, the axioelectric coupling constant g_{Ae}, and the dark photon kinetic mixing parameter κ. We also set the first dark matter direct-detection constraints on the mixing angle |U_{e4}|^{2} for keV/c^{2} sterile neutrinos.

Constraints on Sub-GeV Dark-Matter-Electron Scattering from the DarkSide-50 Experiment.

We present new constraints on sub-GeV dark-matter particles scattering off electrons based on 6780.0 kg d of data collected with the DarkSide-50 dual-phase argon time projection chamber. This analysis uses electroluminescence signals due to ionized electrons extracted from the liquid argon target. The detector has a very high trigger probability for these signals, allowing for an analysis threshold of three extracted electrons, or approximately 0.05 keVee. We calculate the expected recoil spectra for dark matter-electron scattering in argon and, under the assumption of momentum-independent scattering, improve upon existing limits from XENON10 for dark-matter particles with masses between 30 and 100 MeV/c^{2}.

Low-Mass Dark Matter Search with the DarkSide-50 Experiment.

We present the results of a search for dark matter weakly interacting massive particles (WIMPs) in the mass range below 20 GeV/c^{2} using a target of low-radioactivity argon with a 6786.0 kg d exposure. The data were obtained using the DarkSide-50 apparatus at Laboratori Nazionali del Gran Sasso. The analysis is based on the ionization signal, for which the DarkSide-50 time projection chamber is fully efficient at 0.1 keVee. The observed rate in the detector at 0.5 keVee is about 1.5 event/keVee/kg/d and is almost entirely accounted for by known background sources. We obtain a 90% C.L. exclusion limit above 1.8 GeV/c^{2} for the spin-independent cross section of dark matter WIMPs on nucleons, extending the exclusion region for dark matter below previous limits in the range 1.8-6 GeV/c^{2}.

Molecular genetics of Delta, a locus required for ectodermal differentiation in Drosophila.

Delta (Dl) is one of the six known zygotic neurogenic genes, each of which is essential for proper segregation of the embryonic ectoderm into neural and epidermal lineages. Molecular analysis of Dl reveals that it is a transcriptionally complex locus that yields multiple maternal and zygotic transcripts. DNA sequence analysis suggests that the predominant product of the locus is a putative transmembrane protein exhibiting homology to blood coagulation factors and epidermal growth factor of vertebrates. The structure of this product is consistent with the hypothesis that Dl participates in cell-cell interactions that are central to establishment of the epidermal lineage within the developing ectoderm. Genetic analyses demonstrate that Dl mutations can modify the imaginal phenotypes that result from heterozygosity for Notch (N) mutations as well as the interaction between particular alleles of Notch (N) and Enhancer of split [E(spl)], two other members of the neurogenic gene set. Vital interactions also occur between Dl and N. Given the structures of products encoded by N, Dl, and E(spl), we suggest that the synergistic phenotypic interactions observed among mutations in these three loci result from physical, as opposed to regulatory, interactions.

Delta, a Drosophila neurogenic gene, is transcriptionally complex and encodes a protein related to blood coagulation factors and epidermal growth factor of vertebrates.

Delta (D1) is required for normal segregation of the embryonic ectoderm into neural and epidermal cell lineages in Drosophila melanogaster. Loss-of-function mutations in D1 and other zygotic neurogenic loci lead to expansion of the neuroblast population at the expense of the dermoblast population within the ectoderm. Characterization of the transcriptional organization and maternal/embryonic expression within the chromosomal interval corresponding to D1 reveals that the locus encodes multiple transcripts: a minimum of two maternal transcripts, approximately 4.5 and 3.6 kb in length, and four zygotic transcripts, approximately 5.4 (two distinct species), 3.5, and 2.8 kb in length. These transcripts differ on the bases of differential splicing and differential polyadenylation site choice. The DNA sequence of a cDNA clone representing the predominant transcripts of the locus indicates that D1 encodes a transmembrane protein homologous to blood coagulation factors and epidermal growth factor. The relationship between coding sequences and transcript-specific exons within the locus suggests that D1 encodes multiple translational products.

Cytogenetic definition and morphogenetic analysis of Delta, a gene affecting neurogenesis in Drosophila melanogaster.

We have conducted a genetic analysis of a small interval of the third chromosome known to include Delta (Dl), a locus that affects the segregation of the ectoderm into neural and epidermal lineages during embryogenesis and the morphogenesis of some ectodermally derived structures, in Drosophila melanogaster. This analysis has led to the definition of seven independent complementation groups, one of which is Delta, within the interval extending from 91F6-13 to 92A2. Among the extant mutations in these seven loci, only mutations in Dl lead to the so-called neurogenic phenotype: hypertrophy of the nervous system and reduction of the epidermis. Combined cytogenetic and genetic analyses allow us to define absolute proximal (91F5-92A1) and distal (92A2) cytogenetic limits for the Dl locus. We have isolated hypomorphic and amorphic alleles of Dl and find that, for any given allele, there is an inverse correlation between neural hypertrophy and epidermal reduction in embryos and a direct correlation between the severity of embryonic phenotypes in mutant homozygotes and hemizygotes and the imaginal phenotype in heterozygous adults.

Characterization of an antigen present on testicular cells and preimplantation embryos whose expression is modified by the t12 haplotype.

In attempts to identify cell surface molecules specified by lethal genes in the T/t-complex, we prepared a rabbit antiserum that has cytotoxic activity against testicular cells from males heterozygous for t12, but not against wild type cells. However, anti-t12 serum immunoprecipitates the same major component, a glycoprotein of mol. wt. 87,000 daltons, from galactose-labelled C3H. +/t12 testicular cell lysate and from congenic C3H. +/+ lysate, although the gp87 molecule precipitated from +/t12 cells appears to be more highly galactosylated than the +/+ form. The antigen is heavily glycosylated in both genotypes, since when testicular cells are treated with tunicamycin before immunoprecipitation, a protein of 40,000-42,000 daltons is obtained. Gp87 is also present on pre-implantation embryos, and on teratocarcinoma cells, but is barely detectable on any adult somatic cells examined. Its expression is developmentally regulated during pre-implantation stages, but the temporal pattern of its expression appears to be different between wild type and t12 embryos. Thus, we believe we have identified a molecule that may play a role in the differentiation of testicular cells and pre-implantation embryos, and that is either specified by genes in the t12 haplotype, or responsive in some way to the effects of t12.

Reexpression of a T/t-complex antigen (t12) in thymocyte x embryonal carcinoma cell hybrids.

Hybrids between PCC4 aza 1 teratocarcinoma cells and thymocytes from an adult +/t12 mouse are phenotypically embryonal carcinoma cells. They express the t 12 antigen and do not express detectable H-2 antigens. Normally t12 is only expressed early in development and on male germ cells. Thus, the thymocyte genome is reprogramed such that adult thymocyte H-2 antigen is turned off but the thymocyte genome participates in the embryonal cell phenotype by reexpressing an embryonic antigen long silent in the adult. The expression of the t12 embryonic antigen represents the first example of the activation of a gene in somatic cell hybrids that is expressed only temporally in development.

Molecular analysis of the genetic relationship of trans interacting factors at the T/t complex.

The T/t complex is an extensive genetic region proximal to the H-2 complex on mouse chromosome 17, with multiple effects on embryonic development, spermatogenesis and recombination. Recently, two-dimensional gel analysis of testicular cell proteins identified a gene within the T/t complex that codes for a major cell surface-associated protein, p63/6.9 (ref. 4). The wild-type gene, Tcp-1b, codes for a 63,000-molecular weight protein (p63/6.9b), whereas a mutant allele, Tcp-1a, which occurs in all intact t haplotypes, codes for a more acidic form of the protein (p63/6.9a). Analysis of partial t haplotypes obtained from rare recombination events showed that Tcp-1a correlated completely with the tail interaction factor tT, which is thought to be a genetic allele of T, thus raising the possibility that the locus of T codes for the p63/6.9 protein. We report here that the p63/6.9 proteins produced by seven chromosomes carrying independently derived dominant mutations at the locus of T are all indistinguishable from the wild-type form; thus, the cumulative data indicate that the Tcp-1 gene is most probably not at the locus of T.