Diversity of the subgenus Disparalona (Mixopleuroxus) Hudec, 2010 (Crustacea: Cladocera) in the New and Old World

During the last three decades, strong progress was made in the taxonomy of the family Chydoridae (Crustacea: Cladocera), and the results of these revisions have become a valuable confirmation of the non-cosmopolitanism in the cladoceran distribution. But, to date, delineation between several chydorid genera (Pleuroxus Baird, 1843, Picripleuroxus Frey, 1993, Alonella Sars, 1862 and Disparalona Fryer, 1968) has been intuitive rather than based on careful diagnostics. Disparalona is a cladoceran genus with a complicated and confused taxonomy. We compiled a checklist of all formal taxa belonging to this genus in current understanding. Our study comprises a taxonomic revision of the North American, African and East Asian populations of D. cf. hamata with the aim of clarifying their species and generic status. We redescribe D. hamata (Birge, 1879) based on material from North America and D. chappuisi (Brehm, 1934) based on material from Africa. The latter is common in tropical–subtropical Asia, with a distribution range reaching the Far East of Russia. The second taxon from Africa is provisionally identified as D. cf. striatoides (?rámek-Hu?ek, 1946), which was described initially from the Czech Republic. Further comparison is needed for a final conclusion on conspecifity of European and African populations provisionally placed to this taxon. At the current level of knowledge Mixopleuroxus Hudec, 2010 must be accepted as a subgenus of the genus Disparalona. The diagnoses of Disparalona s. str. and D. (Mixopleuroxus) are provided. Disparalona s. str. includes D. ikarus Kotov and Sinev, 2011, D. leei (Chien Shing-ming, 1970), D. rostrata (Koch, 1841) and D. smirnovi Sinev, 2015, while D. (Mixopleuroxus) includes D. hamata, D. chappuisi and D. striatoides. D. leptorhyncha (Daday, 1905) and D. caudata Smirnov, 1996 are not described adequately, but they also probably belong to the latter subgenus. The status of D. acutirostris (Birge, 1879) must be clarified in the future.

www.zoobank.org/urn:lsid:zoobank.org:pub:971811AE-DF72-47E9-AED9-DEE835D1D412     

Flagellin glycosylation with pseudaminic acid in <Emphasis Type="Italic">Campylobacter</Emphasis> and <Emphasis Type="Italic">Helicobacter</Emphasis>: prospects for development of novel therapeutics

Many pathogenic bacteria require flagella-mediated motility to colonise and persist in their hosts. Helicobacter pylori and Campylobacter jejuni are flagellated epsilonproteobacteria associated with several human pathologies, including gastritis, acute diarrhea, gastric carcinoma and neurological disorders. In both species, glycosylation of flagellin with an unusual sugar pseudaminic acid (Pse) plays a crucial role in the biosynthesis of functional flagella, and thereby in bacterial motility and pathogenesis. Pse is found only in pathogenic bacteria. Its biosynthesis via six consecutive enzymatic steps has been extensively studied in H. pylori and C. jejuni. This review highlights the importance of flagella glycosylation and details structural insights into the enzymes in the Pse pathway obtained via a combination of biochemical, crystallographic, and mutagenesis studies of the enzyme–substrate and –inhibitor complexes. It is anticipated that understanding the underlying structural and molecular basis of the catalytic mechanisms of the Pse-synthesising enzymes will pave the way for the development of novel antimicrobials.     

The acidic microenvironment as a possible niche of dormant tumor cells

Although surgical excision, chemo-, and radio-therapy are clearly advanced, tumors may relapse due to cells of the so-called “minimal residual disease”. Indeed, small clusters of tumor cells persist in host tissues after treatment of the primary tumor elaborating strategies to survive and escape from immunological attacks before their relapse: this variable period of remission is known as “cancer dormancy”. Therefore, it is crucial to understand and consider the major concepts addressing dormancy, to identify new targets and disclose potential clinical strategies. Here, we have particularly focused the relationships between tumor microenvironment and cancer dormancy, looking at a re-appreciated aspect of this compartment that is the low extracellular pH. Accumulating evidences indicate that acidity of tumor microenvironment is associated with a poor prognosis of tumor-bearing patients, stimulates a chemo- and radio-therapy resistant phenotype, and suppresses the tumoricidal activity of cytotoxic lymphocytes and natural killer cells, and all these aspects are useful for dormancy. Therefore, this review discusses the possibility that acidity of tumor microenvironment may provide a new, not previously suggested, adequate milieu for “dormancy” of tumor cells.     

A novel 72-kDa leukocyte-derived osteoglycin enhances the activation of toll-like receptor 4 and exacerbates cardiac inflammation during viral myocarditis

Background

Viral myocarditis can severely damage the myocardium through excessive infiltration of immune cells. Osteoglycin (OGN) is part of the small leucine-rich repeat proteoglycan (SLRP) family. SLRP’s may affect inflammatory and fibrotic processes, but the implication of OGN in cardiac inflammation and the resulting injury upon viral myocarditis is unknown.

Methods and results

This study uncovered a previously unidentified 72-kDa variant of OGN that is predominant in cardiac human and mouse samples of viral myocarditis. Its absence in mice significantly decreased cardiac inflammation and injury in Coxsackievirus-B3-induced myocarditis. It also delayed mortality in lipopolysaccharide-induced endotoxemia going along with a reduced systemic production of pro-inflammatory cytokines. This 72-kDa OGN is expressed in the cell membrane of circulating and resident cardiac macrophages and neutrophils. Co-immunoprecipitation and OGN siRNA experiments revealed that this 72-kDa variant activates the toll-like receptor-4 (TLR4) with a concomitant increase in IL-6, TNF-α, IL-1β, and IL-12 expression. This immune cell activation by OGN occurred via MyD88 and increased phosphorylation of c-jun. Finally, the 72-kDa chondroitin sulfate is the result of O-linked glycosylation of the 32-kDa protein core of OGN. In contrast, the 34-kDa dermatan sulfate-OGN, involved in collagen cross linking, was also the result of O-linked glycosylation.

Conclusion

The current study discovered a novel 72-kDa chondroitin sulfate-OGN that is specific for innate immune cells. This variant is able to bind and activate TLR4. The absence of OGN decreases cytokine production by both circulating and cardiac leukocytes upon (systemic) LPS exposure, and reduces cardiac inflammation and injury in viral myocarditis.

     

Nesting ecology of waterbirds at Grays Lake, Idaho

Montane wetlands provide valuable habitat for nesting waterfowl and other waterbirds in the western United States, but relatively little information is available about the nesting ecology of their waterbird communities. We describe the general nesting ecology of breeding waterbirds at a large, shallow, montane wetland in southeastern Idaho during 1997-2000. Habitats include upland grasslands and intermittently to semipermanently flooded wetland habitats. We located a total of 1207 nests of 23 bird species: Eared Grebe ( Podiceps nigricollis ), Canada Goose ( Branta canadensis ), Mallard ( Anas platyrhynchos ), Gadwall ( A. strepera ), American Wigeon ( A. americana ), Green-winged Teal ( A. crecca ), Blue-winged Teal ( A. discors ), Cinnamon Teal ( A. cyanoptera ), Northern Shoveler ( A. clypeata ), Northern Pintail ( A. acuta ), Redhead ( Aythya americana ), Canvasback ( A. valisineria ), Lesser Scaup ( A. affinis ), Ruddy Duck ( Oxyura jamaicensis ), Northern Harrier ( Circus cyaneus ), American Coot ( Fulica americana ), Virginia Rail ( Rallus limicola ), Greater Sandhill Crane ( Grus canadensis tabida ), American Avocet ( Recurvirostra americana ), Long-billed Curlew ( Numenius americanus ), Wilson's Snipe ( Gallinago delicata ), Wilson's Phalarope ( Phalaropus tricolor ), and Short-eared Owl ( Asio flammeus ). Most nests were initiated in May-early June and were terminated (hatched or destroyed) by the 3rd week of June. Mean daily survival rate (DSR) for Canada Goose nests was 0.954 ± 0.005 ( s ￣x ; n = 127 nests), equivalent to Mayfield nest success of 21%. Mean DSR for dabbling duck nests over all 4 years was 0.938 ± 0.006 ( n = 41), equivalent to Mayfield nest success of 11%. For all other species where we found > 10 nests each year (Eared Grebe, Redhead, Canvasback, Coot, Sandhill Crane, American Avocet, and Wilson's Snipe), > 50% of nests found hatched at least 1 young. Success rates for geese, cranes, and ducks were lower than reported for Grays Lake during 1949-1951 and lower than most other wetlands in the region.     

Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47

Genome-wide association studies and candidate gene studies in ulcerative colitis have identified 18 susceptibility loci. We conducted a meta-analysis of six ulcerative colitis genome-wide association study datasets, comprising 6,687 cases and 19,718 controls, and followed up the top association signals in 9,628 cases and 12,917 controls. We identified 29 additional risk loci (P < 5 × 10(-8)), increasing the number of ulcerative colitis-associated loci to 47. After annotating associated regions using GRAIL, expression quantitative trait loci data and correlations with non-synonymous SNPs, we identified many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1. The total number of confirmed inflammatory bowel disease risk loci is now 99, including a minimum of 28 shared association signals between Crohn's disease and ulcerative colitis.     

Mutations in ORC1, encoding the largest subunit of the origin recognition complex, cause microcephalic primordial dwarfism resembling Meier-Gorlin syndrome

Studies into disorders of extreme growth failure (for example, Seckel syndrome and Majewski osteodysplastic primordial dwarfism type II) have implicated fundamental cellular processes of DNA damage response signaling and centrosome function in the regulation of human growth. Here we report that mutations in ORC1, encoding a subunit of the origin recognition complex, cause microcephalic primordial dwarfism resembling Meier-Gorlin syndrome. We establish that these mutations disrupt known ORC1 functions including pre-replicative complex formation and origin activation. ORC1 deficiency perturbs S-phase entry and S-phase progression. Additionally, we show that Orc1 depletion in zebrafish is sufficient to markedly reduce body size during rapid embryonic growth. Our data suggest a model in which ORC1 mutations impair replication licensing, slowing cell cycle progression and consequently impeding growth during development, particularly at times of rapid proliferation. These findings establish a novel mechanism for the pathogenesis of microcephalic dwarfism and show a surprising but important developmental impact of impaired origin licensing.     

Candidate lung tumor susceptibility genes identified through whole-genome association analyses in inbred mice

We performed a whole-genome association analysis of lung tumor susceptibility using dense SNP maps ( approximately 1 SNP per 20 kb) in inbred mice. We reproduced the pulmonary adenoma susceptibility 1 (Pas1) locus identified in previous linkage studies and further narrowed this quantitative trait locus (QTL) to a region of less than 0.5 Mb in which at least two genes, Kras2 (Kirsten rat sarcoma oncogene 2) and Casc1 (cancer susceptibility candidate 1; also known as Las1), are strong candidates. Casc1 knockout mouse tumor bioassays showed that Casc1-deficient mice were susceptible to chemical induction of lung tumors. We also found three more genetic loci for lung adenoma development. Analysis of one of these candidate loci identified a previously uncharacterized gene Lasc1, bearing a nonsynonymous substitution (D102E). We found that the Lasc1 Glu102 allele preferentially promotes lung tumor cell growth. Our findings demonstrate the prospects for using dense SNP maps in laboratory mice to refine previous QTL regions and identify genetic determinants of complex traits.