Five new species and three new subspecies of Erebidae and Noctuidae (Insecta, Lepidoptera) from Northwestern North America, with notes on Chytolita Grote (Erebidae) and Hydraecia Guenée (Noctuidae)

This is the publisher’s final pdf. The published article is copyrighted by Pensoft Publishers and can be found at: http://www.pensoft.net/journals/zookeys/.Several taxonomic issues in the moth families Erebidae and Noctuidae are addressed for Northwestern North America. Drasteria parallela Crabo & Mustelin and Cycnia oregonensis tristis Crabo in the Erebidae and Eudryas brevipennis bonneville Shepard & Crabo, Resapamea diluvius Crabo, Resapamea angelika Crabo, Resapamea mammuthus Crabo, Fishia nigrescens Hammond & Crabo, and Xestia perquiritata orca Crabo & Hammond in the Noctuidae are described as new. The following new synonyms are proposed: Chytolita petrealis Grote with Herminea morbidalis Guenee; Gortyna columbia Barnes & Benjamin and Gortyna ximena Barnes & Benjamin with Gortyna obliqua Harvey; and Hydroecia pallescens Smith with Hydroecia medialis Smith. The type locality of Gortyna intermedia Barnes & Benjamin is restricted to Lundbreck, Municipality of Crowsnest Pass, Alberta, Canada

Differential phosphorylation of NG2 proteoglycan by ERK and PKCα helps balance cell proliferation and migration

Two distinct Thr phosphorylation events within the cytoplasmic domain of the NG2 proteoglycan help regulate the cellular balance between proliferation and motility. Protein kinase Cα mediates the phosphorylation of NG2 at Thr2256, resulting in enhanced cell motility. Extracellular signal–regulated kinase phosphorylates NG2 at Thr2314, stimulating cell proliferation. The effects of NG2 phosphorylation on proliferation and motility are dependent on β1-integrin activation. Differential cell surface localization of the two distinctly phosphorylated forms of NG2 may be the mechanism by which the NG2–β1-integrin interaction promotes proliferation in one case and motility in the other. NG2 phosphorylated at Thr2314 colocalizes with β1-integrin on microprotrusions from the apical cell surface. In contrast, NG2 phosphorylated at Thr2256 colocalizes with β1-integrin on lamellipodia at the leading edges of cells. Thus, phosphorylation and the resulting site of NG2–integrin localization may determine the specific downstream effects of integrin signaling

Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus

A hallmark of systemic lupus erythematosus (SLE), and several related autoimmune diseases, is the presence of autoantibodies against nucleic acids and nucleic acid-binding proteins, as well as elevated type I interferons (IFNs), which appear to be instrumental in disease pathogenesis. Here we discuss the sources and proposed mechanisms by which a range of cellular RNA and DNA species can become pathogenic and trigger the nucleic acid sensors that drive type I interferon production. Potentially SLE-promoting DNA may originate from pieces of chromatin, from mitochondria, or from reverse-transcribed cellular RNA, while pathogenic RNA may arise from mis-localized, mis-processed, ancient retroviral, or transposable element-derived transcripts. These nucleic acids may leak out from dying cells to be internalized and reacted to by immune cells or they may be generated and remain to be sensed intracellularly in immune or non-immune cells. The presence of aberrant DNA or RNA is normally counteracted by effective counter-mechanisms, the loss of which result in a serious type I IFN-driven disease called Aicardi-Goutières Syndrome. However, in SLE it remains unclear which mechanisms are most critical in precipitating disease: aberrant RNA or DNA, overly sensitive sensor mechanisms, or faulty counter-acting defenses. We propose that the clinical heterogeneity of SLE may be reflected, in part, by heterogeneity in which pathogenic nucleic acid molecules are present and which sensors and pathways they trigger in individual patients. Elucidation of these events may result in the recognition of distinct “endotypes” of SLE, each with its distinct therapeutic choices

Identification and characterization of DUSP27, a novel dual-specific protein phosphatase

AbstractA novel human dual-specific protein phosphatase (DSP), designated DUSP27, is here described. The DUSP27 gene contains three exons, rather than the predicted 4–14 exons, and encodes a 220 amino acid protein. DUSP27 is structurally similar to other small DSPs, like VHR and DUSP13. The location of DUSP27 on chromosome 10q22, 50kb upstream of DUSP13, suggests that these two genes arose by gene duplication. DUSP27 is an active enzyme, and its kinetic parameters and were determined. DUSP27 is a cytosolic enzyme, expressed in skeletal muscle, liver and adipose tissue, suggesting its possible role in energy metabolism

Low-Molecular-Weight Protein Tyrosine Phosphatases of Bacillus subtilis

In gram-negative organisms, enzymes belonging to the low-molecular-weight protein tyrosine phosphatase (LMPTP) family are involved in the regulation of important physiological functions, including stress resistance and synthesis of the polysaccharide capsule. LMPTPs have been identified also in gram-positive bacteria, but their functions in these organisms are presently unknown. We cloned two putative LMPTPs from Bacillus subtilis, YfkJ and YwlE, which are highly similar to each other in primary structure as well as to LMPTPs from gram-negative bacteria. When purified from overexpressing Escherichia coli strains, both enzymes were able to dephosphorylate p-nitrophenyl-phosphate and phosphotyrosine-containing substrates in vitro but showed significant differences in kinetic parameters and sensitivity to inhibitors. Transcriptional analyses showed that yfkJ was transcribed at a low level throughout the growth cycle and underwent a σB-dependent transcriptional upregulation in response to ethanol stress. The transcription of ywlE was growth dependent but stress insensitive. Genomic deletion of each phosphatase-encoding gene led to a phenotype of reduced bacterial resistance to ethanol stress, which was more marked in the ywlE deletion strain. Our study suggests that YfkJ and YwlE play roles in B. subtilis stress resistance

Expression of L1 retrotransposons in granulocytes from patients with active systemic lupus erythematosus

Background: Patients with systemic lupus erythematosus (SLE) have autoantibodies against the L1-encoded open-reading frame 1 protein (ORF1p). Here, we report (i) which immune cells ORF1p emanates from, (ii) which L1 loci are transcriptionally active, (iii) whether the cells express L1-dependent interferon and interferon-stimulated genes, and (iv) the effect of inhibition of L1 ORF2p by reverse transcriptase inhibitors.Results: L1 ORF1p was detected by flow cytometry primarily in SLE CD66b+CD15+ regular and low-density granulocytes, but much less in other immune cell lineages. The amount of ORF1p was higher in neutrophils from patients with SLE disease activity index (SLEDAI) &gt; 6 (p = 0.011) compared to patients with inactive disease, SLEDAI &lt; 4. Patient neutrophils transcribed seven to twelve human-specific L1 loci (L1Hs), but only 3 that are full-length and with an intact ORF1. Besides serving as a source of detectable ORF1p, the most abundant transcript encoded a truncated ORF2p reverse transcriptase predicted to remain cytosolic, while the two other encoded an intact full-length ORF2p. A number of genes encoding proteins that influence L1 transcription positively or negatively were altered in patients, particularly those with active disease, compared to healthy controls. Components of nucleic acid sensing and interferon induction were also altered. SLE neutrophils also expressed type I interferon-inducible genes and interferon β, which were substantially reduced after treatment of the cells with drugs known to inhibit ORF2p reverse transcriptase activity.Conclusions: We identified L1Hs loci that are transcriptionally active in SLE neutrophils, and a reduction in the epigenetic silencing mechanisms that normally counteract L1 transcription. SLE neutrophils contained L1-encoded ORF1p protein, as well as activation of the type I interferon system, which was inhibited by treatment with reverse transcriptase inhibitors. Our findings will enable a deeper analysis of L1 dysregulation and its potential role in SLE pathogenesis.</p

Five new species and three new subspecies of Erebidae and Noctuidae (Insecta, Lepidoptera) from Northwestern North America, with notes on Chytolita Grote (Erebidae) and Hydraecia Guenée (Noctuidae)

Several taxonomic issues in the moth families Erebidae and Noctuidae are addressed for Northwestern North America. Drasteria parallela Crabo & Mustelin and Cycnia oregonensis tristis Crabo in the Erebidae and Eudryas brevipennis bonneville Shepard & Crabo, Resapamea diluvius Crabo, Resapamea angelika Crabo, Resapamea mammuthus Crabo, Fishia nigrescens Hammond & Crabo, and Xestia perquiritata orca Crabo & Hammond in the Noctuidae are described as new. The following new synonyms are proposed: Chytolita petrealis Grote with Herminea morbidalis Guenee; Gortyna columbia Barnes & Benjamin and Gortyna ximena Barnes & Benjamin with Gortyna obliqua Harvey; and Hydroecia pallescens Smith with Hydroecia medialis Smith. The type locality of Gortyna intermedia Barnes & Benjamin is restricted to Lundbreck, Municipality of Crowsnest Pass, Alberta, Canada

Quantum dot-doped silica nanoparticles as probes for targeting of T-lymphocytes

To enhance diagnostic or therapeutic efficacy, novel nanomaterials must be engineered to function in biologically relevant environments, be visible by conventional fluorescent microscopy, and have multivalent loading capacity for easy detection or effective drug delivery. Here we report the fabrication of silica nanoparticles doped with quantum dots and superficially functionalized with amino and phosphonate groups. The amino groups were acylated with a water-soluble biotin-labeling reagent. The biotinylated nanoparticles were subsequently decorated with neutravidin by exploiting the strong affinity between neutravidin and biotin. The resultant neutravidin-decorated fluorescent silica nanoparticles stably dispersed under physiological conditions, were visible by conventional optical and confocal fluorescent microscopy, and could be further functionalized with macromolecules, nucleic acids, and polymers. We also coated the surface of the nanoparticles with biotinylated mouse anti-human CD3 (αCD3). The resultant fluorescent nanoassembly was taken up by Jurkat T cells through receptor-mediated endocytosis and was partially released to lysosomes. Thus, quantum dot-doped silica nanoparticles decorated with neutravidin represent a potentially excellent scaffold for constructing specific intracellular nanoprobes and transporters

IgG and IgA autoantibodies against L1 ORF1p expressed in granulocytes correlate with granulocyte consumption and disease activity in pediatric systemic lupus erythematosus

BACKGROUND: Most patients with systemic lupus erythematosus (SLE) have IgG autoantibodies against the RNA-binding p40 (ORF1p) protein encoded by the L1 retroelement. This study tested if these autoantibodies are also present in children with pediatric SLE (pSLE) and if the p40 protein itself could be detected in immune cells. METHODS: Autoantibodies in the plasma of pSLE patients (n = 30), healthy children (n = 37), and disease controls juvenile idiopathic arthritis (JIA) (n = 32) and juvenile dermatomyositis (JDM) (n = 60), were measured by ELISA. Expression of p40 in immune cells was assessed by flow cytometry. Markers of neutrophil activation and death were quantitated by ELISA. RESULTS: IgG and IgA autoantibodies reactive with p40 were detected in the pSLE patients, but were low in healthy controls and in JIA or JDM. pSLE patients with active disease (13 of them newly diagnosed) had higher titers than the same patients after effective therapy (p = 0.0003). IgG titers correlated with SLEDAI (r = 0.65, p = 0.0001), ESR (r = 0.43, p = 0.02), and anti-dsDNA antibodies (r = 0.49, p < 0.03), and inversely with complement C3 (r = -0.55, p = 0.002) and C4 (r = -0.51, p = 0.006). p40 protein was detected in a subpopulation of CD66b(+) granulocytes in pSLE, as well as in adult SLE patients. Myeloperoxidase and neutrophil elastase complexed with DNA and the neutrophil-derived S100A8/A9 were elevated in plasma from pSLE patients with active disease and correlated with anti-p40 autoantibodies and disease activity. CONCLUSIONS: Children with active SLE have elevated IgG and IgA autoantibodies against L1 p40, and this protein can be detected in circulating granulocytes in both pediatric and adult SLE patients. P40 expression and autoantibody levels correlate with disease activity. Markers of neutrophil activation and death also correlate with these autoantibodies and with disease activity, suggesting that neutrophils express L1 and are a source of p40. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13075-021-02538-3