base change
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A new coccoid cyanobacterium Aliterella vladivostokensis sp. nov. was described from an urban aerophytic habitat in a temperate monsoon climate (Vladivostok, Russia) using a polyphasic approach. Phylogenetic analyses based on the 16S rRNA gene sequences confirmed that our isolate was a member of the Aliterella genus clade. Aliterella species are hardly distinguishable from each other morphologically and were described from highly contrasting natural and artificial environments with only a few records from several continents. Despite high similarity of morphometric data for A. vladivostokensis and A. antarctica cells and a compensatory base change in the D1–D1′ helix shared by these species; high percent of dissimilarity (11.6±1.3) between their 16S–23S internal transcribed spacer sequences with at least 5 autapomorphic mutations in the D1–D1′ and Box-B helices, and distinct folding patterns of the Box-B helix allowed us to erect a new species.

Abstract Let $f\colon X\to B$ be a semistable fibration where X is a smooth variety of dimension $n\geq 2$ and B is a smooth curve. We give the structure theorem for the local system of the relative $1$ -forms and of the relative top forms. This gives a neat interpretation of the second Fujita decomposition of $f_*\omega _{X/B}$ . We apply our interpretation to show the existence, up to base change, of higher irrational pencils and on the finiteness of the associated monodromy representations under natural Castelnuovo-type hypothesis on local subsystems. Finally, we give a criterion to have that X is not of Albanese general type if $B=\mathbb {P}^1$ .

By computing the completely bounded norm of the flip map on the Haagerup tensor product [Formula: see text] associated to a pair of continuous mappings of locally compact Hausdorff spaces [Formula: see text], we establish a simple characterization of the Beck-Chevalley condition for base change of operator modules over commutative [Formula: see text]-algebras, and a descent theorem for continuous fields of Hilbert spaces.

Hyaluronic acid is a high molecular weight polysaccharide that is widely distributed in animal tissues. Bacterial hyaluronidases degrade hyaluronic acid as secreted enzymes and have been shown to contribute to infection. <i>Staphylococcus aureus</i> UAMS-1 is a clinical isolate that codes for two hyaluronidases (<i>hysA1</i> and <i>hysA2</i>). Previous research has shown the presence of a full-length HysA1 protein from the <i>S. aureus</i> UAMS-1 strain with no evidence of enzymatic activity. A single base change resulting in an E480G amino acid change was identified in the <i>S. aureus</i> UAMS-1 <i>hysA1</i> gene when compared to the <i>S. aureus</i> Sanger 252 <i>hysA1</i> gene. A plasmid copy of the <i>S. aureus</i> Sanger 252 <i>hysA1 </i>gene transduced into a <i>hysA2 </i>deletion mutant strain of <i>S. aureus</i> UAMS-1 restored near wild type levels of enzymatic activity. Homology modeling and structural analysis suggested that Glu-480 in the HysA1 is critically responsible for maintaining the structural and functional ensemble of the catalytic and tunnel-forming residues, which are essential for enzyme activity. A high degree of relatedness among several Gram-positive bacterial hyaluronidases indicate the loss of enzymatic activity of HysA1 in the <i>S. aureus</i> UAMS-1 strain is most likely caused by the mutation identified in our study.

Let [Formula: see text] be a newform of even weight [Formula: see text] for [Formula: see text], where [Formula: see text] is a possibly split indefinite quaternion algebra over [Formula: see text]. Let [Formula: see text] be a quadratic imaginary field splitting [Formula: see text] and [Formula: see text] an odd prime split in [Formula: see text]. We extend our theory of [Formula: see text]-adic measures attached to the power series expansions of [Formula: see text] around the Galois orbit of the CM point corresponding to an embedding [Formula: see text] to forms with any nebentypus and to [Formula: see text] dividing the level of [Formula: see text]. For the latter we restrict our considerations to CM points corresponding to test objects endowed with an arithmetic [Formula: see text]-level structure. Also, we restrict these [Formula: see text]-adic measures to [Formula: see text] and compute the corresponding Euler factor in the formula for the [Formula: see text]-adic interpolation of the “square roots”of the Rankin–Selberg special values [Formula: see text], where [Formula: see text] is the base change to [Formula: see text] of the automorphic representation of [Formula: see text] associated, up to Jacquet-Langland correspondence, to [Formula: see text] and [Formula: see text] is a compatible family of grössencharacters of [Formula: see text] with infinite type [Formula: see text].

AbstractLet K be an imaginary quadratic field. In this article, we study the eigenvariety for $$\mathrm {GL}_2/K$$ GL 2 / K , proving an étaleness result for the weight map at non-critical classical points and a smoothness result at base-change classical points. We give three main applications of this; let f be a p-stabilised newform of weight $$k \ge 2$$ k ≥ 2 without CM by K. Suppose f has finite slope at p and its base-change $$f_{/K}$$ f / K to K is p-regular. Then: (1) We construct a two-variable p-adic L-function attached to $$f_{/K}$$ f / K under assumptions on f that conjecturally always hold, in particular with no non-critical assumption on f/K. (2) We construct three-variable p-adic L-functions over the eigenvariety interpolating the p-adic L-functions of classical base-change Bianchi cusp forms. (3) We prove that these base-change p-adic L-functions satisfy a p-adic Artin formalism result, that is, they factorise in the same way as the classical L-function under Artin formalism.

Quantitative trait locus mapping for interleukin-1β release after inflammasome priming and activation was performed on bone-marrow-derived macrophages (BMDM) from an AKRxDBA/2 mouse strain intercross. The strongest associated locus mapped very close to the Pycard gene on chromosome 7, which codes for the inflammasome adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC). The DBA/2 and AKR Pycard genes only differ at a single-nucleotide polymorphism (SNP) in their 3’ untranslated region (UTR). DBA/2 vs. AKR BMDM had increased levels of Pycard mRNA expression and ASC protein, and increased inflammasome speck formation, which was associated with increased Pycard mRNA stability without an increased transcription rate. CRISPR/Cas9 gene editing was performed on DBA/2 embryonic stem cells to change the Pycard 3’UTR SNP from the DBA/2 to the AKR allele. This single base change significantly reduced Pycard expression and inflammasome activity after cells were differentiated into macrophages due to reduced Pycard mRNA stability.

AbstractMany single nucleotide variants (SNVs) associated with human traits and genetic diseases are thought to alter the activity of existing regulatory elements. Some SNVs may also create entirely new regulatory elements which change gene expression, but the mechanism by which they do so is largely unknown. Here we show that a single base change in an otherwise unremarkable region of the human α-globin cluster creates an entirely new promoter and an associated unidirectional transcript. This SNV downregulates α-globin expression causing α-thalassaemia. Of note, the new promoter lying between the α-globin genes and their associated super-enhancer disrupts their interaction in an orientation-dependent manner. Together these observations show how both the order and orientation of the fundamental elements of the genome determine patterns of gene expression and support the concept that active genes may act to disrupt enhancer-promoter interactions in mammals as in Drosophila. Finally, these findings should prompt others to fully evaluate SNVs lying outside of known regulatory elements as causing changes in gene expression by creating new regulatory elements.