Little-known and phylogenetically obscure South African estuarine microgastropods (Mollusca: Truncatelloidea) as living animals

Areas of the Knysna estuarine bay in the Western Cape are dominated by three endemic South African truncatelloid microgastropods, temporarily known as ‘Hydrobia’ knysnaensis (Krauss), ‘Assiminea’ capensis (Sowerby) and ‘Assiminea’ globulus Connolly. Although first described 80–170 years ago and present in abundance (up to 100,000 m^?2), they remain surrounded by confusion and still await taxonomic assignment, largely because they appear most atypical members of their groups by virtue of anatomy and/or biogeography and/or habitat. This study contributes in-life perspectives to morphological and phylogenetic analyses known to be on-going. At Knysna, they are syntopic: at least two occurring in >85% and all three in >40% of individual 0.0026 m² samples from their region of dominance. Nevertheless, they tend to greater abundance in divergent microhabitats; ‘A.’ globulus dominating higher tidal levels, and ‘A.’ capensis and ‘Hydrobia’ lower ones; the former especially unvegetated sediment, the latter, if anything, seagrass. Interspecific feeding interactions appear unlikely to be responsible for these patterns, other evidence suggesting that all are maintained below carrying capacity. Field biology of ‘H.’ knysnaensis generally appears equivalent to that of northern-hemisphere intertidal hydrobiids and that of ‘A.’ globulus is typically assimineid, albeit at atypically low shore height. Unlike assimineids, however, ‘A.’ capensis is truly aquatic. The success of these truncatelloids in unusual circumstances may be consequent on the absence from South Africa of other microgastropod groups that fill their niches elsewhere in the southern hemisphere.     

Constructing and evaluating core inflation measures from component‐level inflation data

This paper undertakes a comprehensive examination of 10 measures of core inflation and evaluates which measure produces the best forecast of headline inflation out‐of‐sample. We use the Personal Consumption Expenditure Price Index as our measure of inflation. We use two sets of components (17 and 50) of the Personal Consumption Expenditure Price Index to construct these core inflation measures and evaluate these measures at the three time horizons (6, 12 and 24 months) most relevant for monetary policy decisions. The best measure of core inflation for both sets of components and over all time horizons uses weights based on the first principal component of the disaggregated (component‐level) prices. Interestingly, the results vary by the number of components used; when more components are used the weights based on the persistence of each component is statistically equivalent to the weights generated by the first principal component. However, those forecasts using the persistence of 50 components are statistically worse than those generated using the first principal component of 17 components. The statistical superiority of the principal component method is due to the fact that it extracts (in the first principal component) the common source of variation in the component level prices that accurately describes trend inflation over the next 6–24 months.     

The modernity of Dedekind’s anticipations contained in What are numbers and what are they good for?

Archive for History of Exact Sciences - We show that Dedekind, in his proof of the principle of definition by mathematical recursion, used implicitly both the concept of an inductive cone from an...     

The expansion of GPCR transactivation-dependent signalling to include serine/threonine kinase receptors represents a new cell signalling frontier

G protein-coupled receptor (GPCR) signalling is mediated through transactivation-independent signalling pathways or the transactivation of protein tyrosine kinase receptors and the recently reported activation of the serine/threonine kinase receptors, most notably the transforming growth factor-β receptor family. Since the original observation of GPCR transactivation of protein tyrosine kinase receptors, there has been considerable work on the mechanism of transactivation and several pathways are prominent. These pathways include the “triple membrane bypass” pathway and the generation of reactive oxygen species. The recent recognition of GPCR transactivation of serine/threonine kinase receptors enormously broadens the GPCR signalling paradigm. It may be predicted that the transactivation of serine/threonine kinase receptors would have mechanistic similarities with transactivation of tyrosine kinase pathways; however, initial studies suggest that these two transactivation pathways are mechanistically distinct. Important questions are the relative importance of tyrosine and serine/threonine transactivation pathways, the contribution of transactivation to overall GPCR signalling, mechanisms of transactivation and the range of cell types in which this phenomenon occurs. The ultimate significance of transactivation-dependent signalling remains to be defined but it appears to be prominent and if so will represent a new cell signalling frontier.     

The Shwachman-Bodian-Diamond syndrome protein mediates translational activation of ribosomes in yeast

The autosomal recessive disorder Shwachman-Diamond syndrome, characterized by bone marrow failure and leukemia predisposition, is caused by deficiency of the highly conserved Shwachman-Bodian-Diamond syndrome (SBDS) protein. Here, we identify the function of the yeast SBDS ortholog Sdo1, showing that it is critical for the release and recycling of the nucleolar shuttling factor Tif6 from pre-60S ribosomes, a key step in 60S maturation and translational activation of ribosomes. Using genome-wide synthetic genetic array mapping, we identified multiple TIF6 gain-of-function alleles that suppressed the pre-60S nuclear export defects and cytoplasmic mislocalization of Tif6 observed in sdo1Delta cells. Sdo1 appears to function within a pathway containing elongation factor-like 1, and together they control translational activation of ribosomes. Thus, our data link defective late 60S ribosomal subunit maturation to an inherited bone marrow failure syndrome associated with leukemia predisposition.