Data standards, sense and stability: Scratchpads, the ICZN and ZooBank

The International Commission of Zoological Nomenclature has used the Scratchpads platform (currently being developed and maintained by ViBRANT) as the foundation for its redesigned website and as a platform for engaging with its users. The existing Scratchpad tools, with extensions to provide additional functions, have allowed for a major transformation in presentation of linked nomenclatural tools. Continued development of the new website will act as a springboard for the ICZN to participate more fully in the wider community of biodiversity informatics.     

The rare Chrysopidae (Neuroptera) of southwestern Europe

Quantitative surveys of the chrysopid fauna from southwestern Europe, namely the Iberian and Italian peninsulas, France south of 46° N, and the west-Mediterranean Islands, were analysed. A total of 56 species of Chrysopidae were reported, of which three species were abundant. These, Chrysoperla carnea (Stephens, 1836) sensu lato, Dichochrysa prasina (Burmeister, 1839) and D. flavifrons (Brauer, 1850), comprised a large percentage of the specimens. For the rarer species, comments are made on their distributions, the enhanced geographic range of exotic ones, and on levels of endemism and stenotopy.     

An evolutionary analytical model of a complementary circular code

The subset X0=[AAC,AAT,ACC,ATC,ATT,CAG,CTC,CTG, GAA,GAC,GAG,GAT,GCC,GGC,GGT,GTA,GTC,GTT,TAC,TTC] of 20 trinucleotides has a preferential occurrence in the frame 0 (reading frame established by the ATG start trinucleotide) of protein (coding) genes of both prokaryotes and eukaryotes. This subset X0 is a complementary maximal circular code with two permutated maximal circular codes X1 and X2 in the frames 1 and 2 respectively (frame 0 shifted by one and two nucleotides respectively in the 5'-3' direction). X0 is called a C3 code (Arquès and Michel, 1997, J. Biosyst 44, 107-134). A quantitative study of these three subsets X0, X1 and X2 in the three frames 0, 1 and 2 of eukaryotic protein genes shows that their occurrence frequencies are constant functions of the trinucleotide positions in the sequences. The frequencies of X0, X1 and X2 in the frame 0 of eukaryotic protein genes are 48.5%, 29% and 22.5% respectively. These properties are not observed in the 5' and 3' regions of eukaryotes where X0, X1 and X2 occur with variable frequencies around the random value (1/3). Several frequency asymmetries unexpectedly observed, e.g. the frequency difference between X1 and X2 in the frame 0, are related to a new property of the C3 code X0 involving substitutions. An evolutionary analytical model at three parameters (p, q, t) based on an independent mixing of the 20 codons (trinucleotides in the frame 0) of X0 with equiprobability (1/20) followed by t approximately 4 substitutions per codon according to the proportions p approximately 0.1, q approximately 0.1 and r = 1 - p - q approximately 0.8 in the three codon sites respectively, retrieves the frequencies of X0, X1 and X2 observed in the three frames of protein genes and explains these asymmetries. The complex behaviour of these analytical curves is totally unexpected and a priori difficult to imagine. Finally, the evolutionary analytical method developed could be applied to the phylogenetic tree reconstruction and the DNA sequence alignment.     

Ultrastructural detection of an unusual intranuclear bacterium in Pentastiridius leporinus (Hemiptera: Cixiidae)

Pentastiridius leporinus is an important vector of sugar beet pathogens in eastern France. An electron microscope survey on the insect-associated microflora revealed the occurrence of intranuclear prokaryotic cells in every internal organ analysed. These bacteria, which could also be found in the cytoplasm surrounding the nucleus, had a homogeneous coccoid (ca. 0.45 microm) or rod (0.45-1 microm) shape. The presence of three membrane layers was observed, the outermost forming a kind of vacuole containing generally a single microorganism. No cytopathological abnormalities were detected in the infected cells. To our knowledge, this is the first report of a hemipteran species infected by intranuclear bacteria. The possible identity of this microorganism is discussed.     

Flagellin/TLR5 signalling activates renal collecting duct cells and facilitates invasion and cellular translocation of uropathogenic Escherichia coli

Uropathogenic Escherichia coli (UPEC) colonizing kidneys is the main cause of acute pyelonephritis. TLR5 that senses flagellin was shown to be highly expressed in the bladder and to participate in host defence against flagellated UPEC, although its role in kidneys still remains elusive. Here we show that TLR5 is expressed in renal medullary collecting duct (MCD) cells, which represent a preferential site of UPEC adhesion. Flagellin, like lipopolysaccharide, stimulated the production of the chemoattractant chemokines CXCL1 and CXCL2, and subsequent migration capacity of neutrophils in cultured wild‐type (WT) and Tlr4^?/? MCDs, but not in Tlr5^?/? MCDs. UPEC can translocate across intact MCD layers without altering tight junctions. Strikingly, the invasion capacity and transcellular translocation of the UPEC strain HT7 were significantly lower in Tlr5^?/? than in WT MCDs. The non‐motile HT7ΔfliC mutant lacking flagellin also exhibited much lower translocation capacities than the HT7 isolates. Finally, Tlr5^?/? kidneys exhibited less infiltrating neutrophils than WT kidneys one day after the transurethral inoculation of HT7, and greater delayed renal bacterial loads in the day 4 post‐infected Tlr5^?/? kidneys. Overall, these findings indicate that the epithelial TLR5 participates to renal antibacterial defence, but paradoxically favours the translocation of UPEC across intact MCD cell layers.     

Hypomorphic mutations in the gene encoding a key Fanconi anemia protein, FANCD2, sustain a significant group of FA-D2 patients with severe phenotype

FANCD2 is an evolutionarily conserved Fanconi anemia (FA) gene that plays a key role in DNA double-strand-type damage responses. Using complementation assays and immunoblotting, a consortium of American and European groups assigned 29 patients with FA from 23 families and 4 additional unrelated patients to complementation group FA-D2. This amounts to 3%-6% of FA-affected patients registered in various data sets. Malformations are frequent in FA-D2 patients, and hematological manifestations appear earlier and progress more rapidly when compared with all other patients combined (FA-non-D2) in the International Fanconi Anemia Registry. FANCD2 is flanked by two pseudogenes. Mutation analysis revealed the expected total of 66 mutated alleles, 34 of which result in aberrant splicing patterns. Many mutations are recurrent and have ethnic associations and shared allelic haplotypes. There were no biallelic null mutations; residual FANCD2 protein of both isotypes was observed in all available patient cell lines. These analyses suggest that, unlike the knockout mouse model, total absence of FANCD2 does not exist in FA-D2 patients, because of constraints on viable combinations of FANCD2 mutations. Although hypomorphic mutations arie involved, clinically, these patients have a relatively severe form of FA.     

l-Phenylalanyl-l-Glutamate-Stimulated, Chloride-Dependent Glutamate Binding Represents Glutamate Sequestration Mediated by an Exchange System

Stimulation of glutamate binding by the dipeptide L-phenylalanyl-L-glutamate (Phe-Glu) was inhibited by the peptidase inhibitor bestatin, suggesting that the stimulation was caused by glutamate liberated from the dipeptide and not by the dipeptide itself. It further suggests that this form of glutamate binding should be reinterpreted as glutamate sequestration and that stimulation of binding both by dipeptides and after preincubation with high concentrations of glutamate is likely to be due to counterflow accumulation. Several other criteria indicate that most of glutamate binding stimulated by chloride represents glutamate sequestration: Binding is reduced when the osmolarity of the incubation medium is increased, when membranes incubated with [3H]glutamate are lysed before filtration, and when membranes are made permeable by transient exposure to saponin. Moreover, dissociation of bound glutamate after a 100-fold dilution of the incubation medium is accelerated about 50 times by the addition of glutamate to the dilution medium. This result would be anomalous if glutamate were bound to a receptor site; it suggests instead that glutamate is transported in and out of membrane vesicles by a transport system that preferentially mediates exchange between internal and external glutamate. Glutamate binding contains a component of glutamate sequestration even when measured in the absence of chloride. Sequestration is adequately abolished only after treating membranes with detergents; even extensive lysis, sonication, and freezing/thawing may be insufficient.     

CD1 molecules efficiently present antigen in immature dendritic cells and traffic independently of MHC class II during dendritic cell maturation

Upon exposure to Ag and inflammatory stimuli, dendritic cells (DCs) undergo a series of dynamic cellular events, referred to as DC maturation, that involve facilitated peptide Ag loading onto MHC class II molecules and their subsequent transport to the cell surface. Besides MHC molecules, human DCs prominently express molecules of the CD1 family (CD1a, -b, -c, and -d) and mediate CD1-dependent presentation of lipid and glycolipid Ags to T cells, but the impact of DC maturation upon CD1 trafficking and Ag presentation is unknown. Using monocyte-derived immature DCs and those stimulated with TNF-alpha for maturation, we observed that none of the CD1 isoforms underwent changes in intracellular trafficking that mimicked MHC class II molecules during DC maturation. In contrast to the striking increase in surface expression of MHC class II on mature DCs, the surface expression of CD1 molecules was either increased only slightly (for CD1b and CD1c) or decreased (for CD1a). In addition, unlike MHC class II, DC maturation-associated transport from lysosomes to the plasma membrane was not readily detected for CD1b despite the fact that both molecules were prominently expressed in the same MIIC lysosomal compartments before maturation. Consistent with this, DCs efficiently presented CD1b-restricted lipid Ags to specific T cells similarly in immature and mature DCs. Thus, DC maturation-independent pathways for lipid Ag presentation by CD1 may play a crucial role in host defense, even before DCs are able to induce maximum activation of peptide Ag-specific T cells.